Documentos de Académico
Documentos de Profesional
Documentos de Cultura
INTERVENTIONAL
RADIOLOGY
with Online Cases
and Videos
KARIM VALJI, MD
Professor of Radiology
Chief of Interventional Radiology
University of Washington
Seattle, Washington
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
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Notices
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Practitioners and researchers must always rely on their own experience and knowledge in
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Valji, Karim.
The practice of interventional radiology : with online cases and videos / Karim Valji.
p. ; cm.
Based on: Vascular and interventional radiology / Karim Valji. 2nd ed. c2006.
Includes bibliographical references and index.
ISBN 978-1-4377-1719-8 (hardcover : alk. paper)
I. Valji, Karim. Vascular and interventional radiology. II. Title.
[DNLM: 1. Radiography, interventionalmethodsAtlases.
2. AngiographymethodsAtlases. 3. Vascular DiseasesradiographyAtlases. WN 17]
LC classification not assigned
616.1307572dc23 2011041700
Printed in China
vii
Preface
For centuries the design and function of medical text- in some depth. Still, the craft of our work can and should
books remained largely unchanged. However, the ongo- only be learned by extensive hands-on training from
ing revolution in digital technology affects almost every experienced practitioners.
human endeavor and its influence on book learning is The book includes over 1500 illustrations, many of
no exception. The rising generation of students and them new. When appropriate, color has been added to
trainees has thoroughly embraced new interactive and radiographic images. All of the line drawings were redone
dynamic educational tools. These materials emphasize in color to improve clarity. References were thoroughly
visual elements, smaller bites of learning, and immedi- updated. The citations are extensive but not exhaustive;
ate access to cited primary sources. For a specialty such they should direct the reader to the most important
as interventional radiology (IR) that is so image-rich and currentas well as classic or historicpublications cover-
procedure driven, the standard printed textbook is be- ing each topic. For many of them, hyperlinks are included
coming an anachronism. There may be heated debate in the web-based version of the book that allow direct
about the merits of the old and new ways, but change is access to the actual journal articles.
unavoidable. The web-based features of this book were The online book format has allowed several new fea-
included to appeal to these new modes for learning IR. tures. The user can access a digital form of the text
The Practice of Interventional Radiology is largely based through the publishers website for use on a computer
on the second edition of my previous text, Vascular and (or, ultimately, an electronic reader). As an e-book, the
Interventional Radiology, which was published in 2006. reader will be able to highlight, dog-ear, and otherwise
Why the title change? Many hospital radiology divisions personalize the content to make it an enduring study
and even the American Board of Radiology still use the guide. A major new element is the online library of over
more traditional term. But almost all young trainees and 100 unknown IR case studies that encompass the essen-
an increasing number of patients around the world call tial diseases and procedures that should be familiar to all
our specialty (in their own native language), quite sim- imagers and interventionalists. The clinical cases and
ply, IR: interventional radiology. The appellation has procedures are completely distinct from those found in
stuck, and we should embrace it. the body of the text. The modules are interactive
As before, my goal is to present the entire spectrum of questions are posed on each screen about the findings on
vascular and nonvascular image-guided interventional the images presented, the differential diagnosis, charac-
procedures in a rigorous but practical, concise, and bal- teristics of the particular disease, and possible treatment
anced fashion. Two new chapters have been added to fill options. More advanced technical questions are aimed at
noticeable gaps in the previous workone covering neu- actual IR practitioners. Each case is ultimately linked to
rointerventional procedures and a second devoted to the appropriate section of the main online text, giving the
interventional oncology. I doubt many readers will miss interested reader more detailed information about the
the one deleted chapter on lymphangiography. The intro- subject under study. The other notable addition is a
ductory section of the book provides a foundation for the collection of short videos comprised of fluoroscopic
discipline, including chapters on the pathology of vascu- sequences and/or movies taken at the interventional
lar diseases (the historic core of IR), the fundamentals table. These subtitled clips illustrate many basic and
of patient care, and basic interventional techniques. The some more complex interventional techniques. Some
bulk of the remaining chapters are clustered in sections videos will be available with the launch of the book;
and cover each of the major vascular beds. The final sec- others will be added over time.
tion contains material on nonvascular interventional pro- The authorship is somewhat unusual for such a
cedures (organized by organ system) and a final chapter broad medical textbook. As with previous editions, I am
on oncologic interventions. Disease pathogenesis and the sole author for the introductory sections and most of
natural history, relevant aspects of imaging studies, the material concerned with vascular interventions. I
specific IR techniques and their expected outcomes, and leave it to the reader to decide whether that was hubris
the relative merits of various treatment modalities are on my part. The nonvascular interventional chapters
emphasized throughout. For every procedure, I have were originally written by IR faculty at the University
summarized the best available evidence to supportor of California, San Diego. All of them have been revised
occasionally refutethe value of a particular therapy. or largely rewritten by colleagues at my new homethe
The technical details of many procedures are described University of Washington in Seattle. Finally, I invited
ix
x PREFACE
several noted authorities from outside institutions to practicing diagnostic radiologists. For interventionalists
write the two new chapters on neurointerventions and finished with primary training, the book should serve as
interventional oncology a comprehensive review of the current state of the field
As before, the book is aimed primarily at trainees in and also as a reference source for occasional consultation.
diagnostic radiology and interventional radiology. The Finally, it may be of value to physicians in other special-
IR fellow should master all of the material set forth in the ties who have an interest in performing selected IR pro-
text. The case library is geared to residents who do not cedures; however, it can only supplement (and certainly
intend to practice the specialty. These individuals still not replace) extensive formal training in these subjects.
need to gain a basic understanding of the nature of
and indications for IR procedures to become competent Karim Valji
Acknowledgments
I am indebted to my publishing team at Elsevier/ book. In addition, a substantial number of the new
Saunders, led by Pam Hetherington, Joanie Milnes, figures come directly from interventional cases they
and Mary Stueck. I am also grateful to David Wolbrecht performed as part of their daily practice.
of UW Creative at the University of Washington for a For two decades, I have had the great pleasure of
first-rate job in editing and producing the video and training interventional radiology fellows and diagnostic
fluoroscopic clips included in the online version of this radiology residents at the University of California, San
book. Diego and the University of Washington. I wrote all of
I am privileged to work with an exceptional group of my books specifically with them in mind. As I have said
colleagues in interventional radiology and vascular sur- before, it is these trainees who keep me feeling young,
gery at the University of Washington and Harborview fresh, and inspired.
Medical Center in Seattle. Many of them enthusiastically
contributed to this project with revised chapters for the Karim Valji
xi
Core Cases in Interventional Radiology
1. Aberrant Right Subclavian Artery (6) 40. Percutaneous Thyroid Biopsy (4)
2. Blue Toe Syndrome from Aortic Plaque (8) 41. Biliary-Enteric Anastomotic Stricture with
3. Normal Upper Extremity Arterial Anatomy (9) Stone Disease (22)
4. Circumaortic Left Renal Vein (10) 42. Leriche Syndrome of Abdominal Aorta (7)
5. Traumatic Leg Arteriovenous Fistula (8) 43. Acute Femoropopliteal Artery Bypass
6. Normal Celiac Artery Anatomy (11) Graft Occlusion (8)
7. Splenic Artery Aneurysm (12) 44. Post-biopsy Renal AV Fistula with
8. Acute Pulmonary Embolism with Thrombolytic Embolotherapy (10)
Therapy (14) 45. Transtracheal Neck Mass Biopsy (4)
9. Percutaneous Cholecystostomy (22) 46. Celiac Compression (Median Arcuate Ligament)
10. Diverticular Abscess Drainage (5) Syndrome (11)
11. Normal Inferior Vena Cava Anatomy (16) 47. Splenic Artery Pseudoaneurysm with
12. Superior Vena Cava Occlusion (17) Embolotherapy (12)
13. Aortic Dissection with Stent Placement (6) 48. Pulmonary AVM with Embolotherapy (14)
14. Abdominal Aortic Aneurysm (AAA) Endovascular 49. Circumaortic Left Renal Vein with IVC Filter
Repair with Type II Endoleak (7) Placement (16)
15. Postoperative Lymphocele Drainage 50. Transgluteal Drainage with Ureteral
and Sclerosis (5) Perforation (5)
16. Biliary Stent Placement for Malignant 51. Acute Secondary Axillosubclavian Vein
Obstruction (22) Thrombosis with Lytic Therapy (17)
17. High Origin of Radial Artery, Variant (9) 52. Aortic Dissection (Stanford A) (6)
18. Renal Artery Stent Placement with Rupture (10) 53. Inflammatory Aortic Aneurysm (7)
19. Separate Origins of Hepatic and Splenic Arteries (11) 54. Pelvic Trauma with Embolotherapy (8)
20. Abdominal Drainage of GIST Tumor (5) 55. Post-transplant Portal Vein Stenosis (12)
21. Uterine Artery Embolization for Fibroid Tumors (13) 56. Hypothenar Hammer Syndrome (9)
22. Bronchial Artery Embolization for Hemoptysis 57. Renal Cell Carcinoma with IVC Invasion (10)
from Tuberculosis (14) 58. Liver Bleeding from Angiosarcoma with
23. Megacava with Filter Placement (16) Embolotherapy (24)
24. Percutaneous Treatment of Ureteral Leak (23) 59. Chronic Left Iliac Vein Occlusion
25. Portal Vein Embolization Prior to Partial Liver (May Thurner Syndrome) (15)
Resection (24) 60. Dialysis Access Balloon Angioplasty (19)
26. Retrieval of Retained Intravascular Foreign Body (18) 61. Port Catheter Tip in Azygous Vein (18)
27. Aortic Coarctation (6) 62. Unusual Thoracic Aortic Aneurysm
28. Thrombosed Popliteal Artery Aneurysm (8) (MAGIC Syndrome) (6)
29. Subclavian Steal Syndrome (9) 63. Percutaneous Treatment of Biliary Stones (22)
30. Retroperitoneal Biopsy of Sarcoma (4) 64. Subclavian and Brachial Artery Embolism
31. Retroaortic Left Renal Vein (10) with Lysis (9)
32. Post-biopsy Colonic Bleed with Embolotherapy (11) 65. Type II Endoleak after Endovascular Aneurysm
33. Treatment of TIPS Dysfunction (12) Repair (7)
34. Pelvic Congestion Syndrome with 66. Blunt Renal Artery Trauma with Embolotherapy (10)
Embolotherapy (13) 67. Chronic Mesenteric Ischemia from SMA
35. Renal Cyst Sclerosis (5) Occlusion (11)
36. Percutaneous Nephrostomy for Ureteral 68. Gastric Varices with Splenorenal Shunt (12)
Obstruction by Stone (23) 69. Adrenal Biopsy (4)
37. Chronic Iliofemoral Vein Thrombosis 70. Popliteal Artery Entrapment (8)
with Stent Placement (15) 71. IVC Duplication with Filter Placement (16)
38. Retrieval of IVC Filter with Retained 72. Cephalic Vein Stenosis with Angioplasty in Patient
Thrombus (16) with Dialysis Graft (19)
39. Superior Vena Cava Syndrome 73. Right Aortic Arch (6)
with Stent Placement (17) 74. Buerger Disease of Lower Extremity (8)
75. Hepatic Amebic Abscess Drainage (5)
Online only at expertconsult.com 76. Renal Artery Fibromuscular Dysplasia
(associated chapters in parentheses). with Angioplasty (10)
xv
xvi CORE CASES IN INTERVENTIONAL RADIOLOGY
77. Jejunal AVM with Chronic Bleeding Treated 96. Degenerative Thoracic Aortic Aneurysm (6)
with Embolotherapy (11) 97. Anastomotic Stenosis of Femoropopliteal
78. TIPS Creation for Portal Hypertension (12) Bypass Graft (8)
79. Hepatocellular Carcinoma with IVC Invasion (24) 98. Primary Chronic Venous Insufficiency
80. Lumbar Artery Bleeding with Embolotherapy (8) with Endovenous Laser Ablation (15)
81. Mycotic Femoral Artery Pseudoaneurysm (8) 99. Popliteal Artery Embolic Occlusion with
82. Blunt Traumatic Occlusion of Renal Artery (10) Lysis (8)
83. Angiomyolipoma of Kidney with Preoperative 100. Chronic Pulmonary Thromboembolic Disease (14)
Embolotherapy (10) 101. Hepatocellular Carcinoma Bleeding with
84. Inferior Vena Cava Occlusion from Embolotherapy (24)
Paraspinal Mass (16) 102. Persistent Sciatic Artery (8)
85. Septic Iliofemoral Vein Thrombus (15) 103. Gastroduodenal Artery Bleeding with
86. Central Venous Catheter Malposition (18) Embolotherapy (11)
87. Renal Artery AVM with Embolotherapy (10) 104. Bleeding from Invasive Molar Pregnancy with
88. Aortic Hypoplasia, William Syndrome (7) Embolotherapy (13)
89. Liver Hemangioma (12) 105. Left Superior Vena Cava (17)
90. Primary Sclerosing Cholangitis Biliary 106. Liver Transplant Hepatic Artery Stenosis with
Drainage (22) Angioplasty (12)
91. Traumatic Aortic Injury with Bovine Arch (6) 107. Left Renal Vein Hypertension with Stent
92. Kidney Transplant Arterial Stenosis Placement (10)
with Stent Placement (10) 108. Blunt Liver Trauma with Embolotherapy for
93. Central Venous In-Stent Restenosis (17) Arterial Bleeding (12)
94. Brachial Artery Occlusion from Penetrating 109. Posttraumatic Subclavian Artery Pseudoaneurysm
Trauma (9) with Embolotherapy (9)
95. Penetrating Aortic Ulcer (6) 110. Hilar Renal Artery Aneurysm (10)
S E C T I O N I
1
Pathogenesis of Vascular Diseases
Karim Valji
Historically, the cornerstone of interventional radiol- The adventitia is composed of a fibrocellular matrix
ogy (IR) is the vascular system, which since the 1950s that includes fibroblasts, collagen, and elastin. In some
was the province of angiographers. Modern IR prac- vessels, an external elastic lamina separates the media
tice now encompasses almost every part of the body. from this outermost layer. Sympathetic nerves penetrate
Although interventionalists must gain a strong foun- into the vessel wall and can alter smooth muscle tone in
dation in the pathology of all organ systems that they the media. A fine network of blood vessels, the vasa
treat, a substantial volume of work still happens within vasorum, supplies the adventitia of larger arteries and
blood vessels. As such, all practitioners engaged in IR, provides nutrients to this layer and the outer media. The
regardless of background, must be particularly expert intima and inner media are nourished by diffusion from
in the pathogenesis of diseases of the arteries and the lumen.
veins. Small arteries become arterioles, which are 40 to
200 micrometers (!m) in diameter. Arterioles lead into
capillaries. Direct arteriovenous communications without
ARTERIES interposed capillary networks exist in some vascular
beds. These connections allow diversion of blood away
from certain parts of the body in physiologic and patho-
Normal Structure logic states, such as shunting of blood from the skin and
Human arteries are composed of three layers (Fig. 1-1). extremities in a hypotensive individual.
The intima consists of a sheet of endothelial cells lining
the vessel lumen and a thin subendothelial matrix. The
endothelium has a variety of critical functions.1 It con-
trols hemostasis largely by acting as a barrier between
circulating blood and the thrombogenic subendothelial
layer. Endothelial cells can indirectly alter vessel caliber
when changes in blood oxygen tension, pressure,
or flow are detected. The endothelium produces and
responds to a variety of factors that are vital to arterial
repair after injury.
The media is separated from the intima by the inter-
nal elastic lamina. This layer is primarily composed
of collagen, elastin, and smooth muscle cells arranged
in longitudinal and circumferential bundles. Elastic
(conduit) arteries (i.e., aorta, aortic arch vessels, iliac
artery, and pulmonary arteries) propel blood forward
because dense bands of elastin let these vessels expand
during systole and contract during diastole.2 In the FIGURE 1-1 Photomicrograph of a normal artery (hematoxylin-
eosin stain, original magnification "40). A single layer of endothelial
smaller-caliber muscular arteries, smooth muscle cells
cells (small arrow) lines the internal elastic lamina (open arrow). The
predominate, and the circumferential orientation of the media is primarily made up of smooth muscle cells (curved arrow).
cells allows the lumen to dilate or constrict in response The external elastic lamina (large arrow) separates the media from the
to various stimuli. adventitia.
3
4 I. BASIC PRINCIPLES AND TECHNIQUES
Functional Disorders
Arterial tone and luminal diameter are regulated by
several mechanisms1:
Cells in the vascular wall release smooth muscle
vasodilators (e.g., prostacyclin, nitric oxide) or
vasoconstrictors (e.g., endothelin, thromboxane
A2) to regulate downstream blood flow.
Vasomotor nerves act through neurotransmitters
such as norepinephrine and acetylcholine.
Circulating agents (e.g., angiotensin II and
vasopressin) also affect vascular tone.
Vasodilation is seen primarily in low-resistance
systems, such as arteriovenous fistulas, arteriovenous
malformations, and hypervascular tumors, and in collat-
eral circulations (Fig. 1-2). Vasoconstriction usually is
the result of vascular trauma or low-flow conditions
(Fig. 1-3). Ingestion or infusion of certain drugs (e.g.,
vasopressin, dopamine, epinephrine) also can lead to
vasospasm (Fig. 1-4). Raynaud disease is a functional disor-
der primarily affecting the small arteries of the hands and
feet in which intermittent vasospasm is caused by external
stimuli3 (see Chapter 9). The hallmarks of vasospasm are
resolution over time or relief with vasodilators.
Arterial standing or stationary waves are an imaging FIGURE 1-2 Enlarged collateral vessels bypass a popliteal artery
curiosity that may be confused with functional vasospasm4 occlusion.
(Fig. 1-5). Standing waves have been noted at both catheter
A B
FIGURE 1-3 Post-traumatic arterial vasospasm. A, The arrow indicates focal narrowing of the upper right brachial artery. B, A follow-up
arteriogram obtained 3 days later shows complete resolution of spasm.
1. PATHOGENESIS OF VASCULAR DISEASES 5
A B
FIGURE 1-4 Vasopressin-induced vasospasm. A, Inferior mesenteric arteriogram shows extravasation in the left colon. B, After infusion of
vasopressin, the vessels are diffusely constricted and the bleeding has stopped.
and magnetic resonance (MR) angiography. Their precise inciting event is endothelial dysfunction mediated through
cause is unknown, but a leading hypothesis invokes sec- the immune system. The damaged endothelium induces
ondary retrograde flow (typical in high resistance arteries) platelet activation, which in turn causes white blood cell
as the explanation for this temporary oscillating pattern.5,6 adhesion to the vascular wall.8 Lipoproteins and mono-
cytes enter the subendothelial space and produce fatty
streaks composed largely of foam cells.9 A variety of fac-
Atherosclerosis
tors are released in response to this pathologic process.
Atherosclerosis is the most common disease affecting the These substances cause medial smooth muscle cells to
vascular system and the leading cause of morbidity and migrate to and then proliferate in the intima. Overproduc-
mortality in the Western world. It develops as a result of an tion of collagen, elastin, and proteoglycans gives the lesion
inflammatory response to lipid storage in the arterial wall.7 a fibrotic character. Chronic inflammation ensues. With time,
Various provocative factors for disease may act as triggers medial thinning, cellular necrosis, and plaque calcification
for inflammation (see later discussion). The common and degeneration occur (Fig. 1-6). Ultimately, plaque frac-
ture, ulceration, hemorrhage, or thrombosis may occur.
A number of risk factors for atherosclerosis have
been identified (Box 1-1). However, these conditions do
A B
FIGURE 1-7 Atherosclerosis. A, Typical diffuse disease involving the abdominal aorta and right iliac artery. There is also thrombotic
occlusion of the left iliac and right internal iliac arteries. B, Focal eccentric narrowing of the popliteal artery.
1. PATHOGENESIS OF VASCULAR DISEASES 7
A B
FIGURE 1-8 Plaque masquerading as thrombus. Lateral aortogram shows apparent embolus in the midabdominal aorta (arrow). B, Frontal
image reveals that the defect is a large polypoid plaque arising from the left side of the aorta (arrow).
Thrombosis
The degree of luminal narrowing (restenosis) after
angioplasty or stent placement depends on the exuber- The ingredients for thrombosis are platelets and other
ance of the neointimal hyperplastic response and the cellular blood elements, coagulation proteins, and often
extent of vascular remodeling. Negative remodeling, an abnormal endothelium. Clot formation begins with
which may be caused by elastic recoil of the vessel or platelet adhesion and aggregation on the subendothelial
progressive thickening of the adventitia, can be partially vascular surface.17 Platelets release substances (e.g.,
controlled by placement of a stent. adenosine diphosphate [ADP] and thromboxane A2)
BOX 1-2
C AU S E S O F A R T E R I A L
LUMINAL NARROWING
Atherosclerosis
Intimal hyperplasia
Vasospasm
Low-flow state
Dissection
Vasculitis FIGURE 1-9 Intimal hyperplasia in a human renal artery
Neoplastic or inflammatory encasement (hematoxylin-eosin stain, original magnification "40). The concentric
Fibromuscular dysplasia thickening of the intima can be identified along with smooth muscle
Extrinsic compression cells, fibroblasts, and matrix material. The internal elastic lamina
(arrow) denotes the boundary between intima and media. (Specimen
courtesy of Ahmed Shabaik, MD, San Diego, Calif.)
8 I. BASIC PRINCIPLES AND TECHNIQUES
A B
FIGURE 1-10 Intimal hyperplasia. A, Aortogram shows narrowing throughout the lumen of a previously placed right renal artery stent
(small arrow). The neointimal hyperplasia is most severe proximally. Incidental note is made of an occluded left renal artery stent and infrarenal
abdominal aortic stenosis (large arrow). B, Following balloon angioplasty, the narrowing of the right renal artery is markedly reduced.
Antiphospholipid syndrome*
Malignancy
Many antitumor and supportive medications Prothrombin gene mutation refers to a single point
(e.g., thalidomide, erythropoietin) defect at the 20210 nucleotide position of the prothrom-
Heparin-induced thrombocytopenia bin gene that causes elevated levels of prothrombin
Myeloproliferative disorders in blood and renders the protein relatively resistant
Polycythemia vera to APC. Like factor V Leiden, this inherited disorder
Essential thrombocythemia only adds significantly to the risk of recurrent
Paroxysmal nocturnal hemoglobinuria VTE when other hypercoagulable risk factors are also
Nephrotic syndrome present.18-20
Inflammatory bowel disease Antithrombin (AT) deficiency is a rare inherited auto-
Advanced age somal dominant disorder expressed as lack of en-
Surgery zyme production (type I) or abnormal enzyme func-
Immobility tion (type II).21 AT is a key protein in regulation
Trauma of coagulation by inactivation of thrombin and a vari-
Obesity ety of other coagulation factors. Although AT defi-
Pregnancy/postpartum state ciency is a rare thrombophilia, it carries a 10- to 30-fold
Estrogen and hormonal therapies (e.g., contracep- increased lifetime relative risk of venous (and less
tives, replacement, selective estrogen receptor often arterial) thrombosis.18,19 An acquired form of
modulators) AT deficiency is associated with liver disease and
Central venous catheters nephrotic syndrome.
Protein C and protein S deficiencies (as measured
*APS may occur as a primary disorder without underlying
systemic lupus erythematosus or other rheumatologic disorder. by activity or serum concentration) may be inherited
or acquired. There is a 75% to 90% lifetime risk for
VTE (and less often arterial thrombosis) in affected indi-
viduals with family members who have suffered a
blunting its natural anticoagulant effect.18 Factor V thrombotic event.19,22 Acquired protein C or S deficiency
Leiden is the most common inherited thrombophilia in can be seen with septic shock, advanced liver disease,
Caucasian populations (about 5%). The lifetime risk for vitamin K antagonists (e.g., warfarin), HIV infection,
venous thromboembolic disease (VTE) for heterozy- nephrotic syndrome, acute inflammation, pregnancy, or
gotes is increased 3- to 8-fold.19 oral contraceptive therapy.
10 I. BASIC PRINCIPLES AND TECHNIQUES
Elevated coagulation factor levels are being recognized patient is a young to middle-aged woman with appar-
as a relatively frequent cause for apparently idiopathic ently idiopathic arterial or venous thrombosis. The risk
thrombophilia. In particular, excessive levels of factors for recurrent thrombotic events is significant. Because
VIII, IX, and XI are associated with increased risk for healthy people may transiently demonstrate aPL anti-
VTE, although specific genetic abnormalities have not bodies, positive clinical and laboratory criteria are
yet been isolated.23,24 needed for diagnosis.
Hyperhomocysteinemia refers to elevated blood levels of Heparin-induced thrombocytopenia (HIT) is triggered
homocysteine, its oxidative metabolite homocystine, and by antibodies to heparin-platelet factor IV complexes
other disulfides.17 A specific mutation in the gene for in blood. These antibody complexes can precipitate
methylenetetrahydrofolate reductase (MTHFR) may platelet activation and degranulation, tissue factor and
cause mild hyperhomocysteinemia. When homocysteine procoagulant release, and ultimately pathologic clot for-
levels are elevated, there is a significant added risk for mation. About 3% of individuals who receive unfraction-
venous or arterial thrombosis.25 Homocystinuria is a rare ated heparin and 1.5% of those who receive low molecular
autosomal recessive disorder caused by mutations of the weight heparin compounds will develop thrombocytope-
cystathionine beta-synthase gene. The illness is marked nia (#50% of baseline) within 4 to 10 days of the start of
by exceedingly high levels of homocysteine, arterial or treatment in any form.28 Up to 50% of these patients will
venous thrombosis at an early age, premature atheroscle- suffer HIT-related thrombosis (HITT), manifested by new
rosis, Marfanoid features, and mental retardation. or worsening VTE, arterial thrombosis, skin necrosis, or
Antiphospholipid syndrome (APS) is the most common catheter-related deep vein thrombosis (DVT).29 When
acquired thrombophilia.17,26 The hallmarks of these bleeding or thrombosis occurs, all heparin products must
conditions are apparently unprovoked vascular throm- be stopped and replaced with a direct thrombin inhibitor.
bosis and persistent elevation of antiphospholipid (aPL) Malignancy-associated hypercoagulability (once called
antibodies of the lupus anticoagulant, anticardiolipin, or Trousseau syndrome) is a multifactorial condition related
anti-beta-2-glycoprotein I type.27 The frequency of to cellular release of procoagulants, tissue factors, cyto-
primary and secondary forms (the latter associated with kines, and platelet activators.30 Cancer is associated with
connective tissue disorders such as systemic lupus impaired fibrinolysis, production of aPL antibodies, and
erythematosus [SLE]) is about equal. The prototypical acquired resistance to APC (Fig. 1-11). Thrombophilia is
A B
FIGURE 1-11 Thrombophilia-induced in situ thrombosis. A, Left leg arteriogram in a young woman with antiphospholipid syndrome
shows an isolated thrombus (arrow). No other vascular disease was found in the legs or pelvis (B).
1. PATHOGENESIS OF VASCULAR DISEASES 11
particularly common in several hematologic malignan- from a plaque.31 Spontaneous release of small atheroem-
cies and in tumors of the pancreas, uterus, ovary, brain, boli cause the blue toe (or blue finger) syndrome. However,
stomach, lung, and prostate.17 the event may be associated with surgical manipulation,
catheterization procedures, or treatment with anticoagu-
lants or fibrinolytic agents.32 Widespread embolization
Embolism into the legs, kidneys, head, or intestinal tract can result in
An embolus is any material that passes through the acute renal failure, stroke, profound lower extremity or
circulation and eventually lodges in a downstream ves- intestinal ischemia, and even death33 (see Chapter 2).
sel. Macroembolism and microembolism of the arterial
circulation have numerous causes (Box 1-7).
Aneurysms and Arterial Dilation
Macroemboli usually are clots that originate from the
heart or a central artery. Atherosclerotic plaque also can An aneurysm is defined as focal or diffuse dilation of an
fragment and obstruct peripheral arteries. Emboli tend to artery by more than 50% of its normal diameter.34 In
lodge at arterial bifurcations or at sites of preexisting dis- a true aneurysm, all three layers of the arterial wall
ease. After the embolic event occurs, the distal arteries are dilated but remain intact (Fig. 1-14). Degenerative
constrict, and new thrombus propagates proximally and (atherosclerosis-associated) aneurysms fall into this
distally to the level of the next large collateral branches.
It may be impossible to differentiate thrombotic from
embolic occlusions by imaging, although an acute em-
bolus has several classic angiographic features (Box 1-8 BOX 1-8
and Fig. 1-12). Real or apparent luminal filling defects are
also observed with intimal flaps, protruding atheroscle- ANGIOGRAPHIC SIGNS
rotic plaques, inflow defects, and rarely with intraluminal O F A C U T E A RT E R I A L
tumor (Fig. 1-13; see also Fig. 1-8). An arterial inflow defect EMBOLISM
is caused by unopacified blood entering an artery beyond
Meniscus or filling defect
an obstruction through a collateral vessel.
Mild or absent diffuse vascular disease
Microemboli are seen in patients with ulcerated, pro-
Lack of contralateral disease (in extremity arteries)
truding atherosclerotic plaques. Platelet-fibrin deposits
Poorly developed collateral circulation
can be released spontaneously into the distal circulation
Emboli or abrupt occlusions at other sites
from a site of underlying disease. Cholesterol crystals
(100 to 200 !) also may shower into the distal circulation
BOX 1-7
S O U R C E S O F A RT E R I A L
EMBOLI
Heart
Left atrial or ventricular thrombus
Endocardial vegetations
Atrial myxoma
Thrombus superimposed on vascular disease
(including aneurysms)
Atherosclerotic plaque
Catheterization procedures
Catheter-related thrombus
Plaque disruption
Gas bubbles
Paradoxical emboli from the venous circulation
Foreign bodies FIGURE 1-12 Acute embolus to the right common/superficial
Catheter or wire fragments femoral artery (large arrow). Note absence of other vascular disease,
Gunshot pellets normal left common femoral artery, and lack of significant collateral
circulation. Also note incidental finding of standing waves in the
right external iliac artery (small arrow).
12 I. BASIC PRINCIPLES AND TECHNIQUES
A B
FIGURE 1-14 A, True degenerative aneurysm of the abdominal aorta with dilation of the entire aortic wall, luminal thrombus, and intimal
calcification (open arrow). B, Maximum intensity projection gadolinium magnetic resonance angiogram shows large infrarenal true abdominal
aortic aneurysm with extension to both iliac arteries.
1. PATHOGENESIS OF VASCULAR DISEASES 13
BOX 1-9
C AU S E S O F A R T E R I A L
A N E U RY S M S FIGURE 1-16 Ehlers-Danlos syndrome, type IV. Diffuse dilation
of the right common iliac artery is noted (arrow) on shaded-surface
display contrast-enhanced computed tomography angiography.
Atherosclerosis-associated degeneration
Trauma
Infection of mural clot, compression of critical arteries (e.g., renal
Inflammation artery), and erosion of adjacent organs. The frequency of
Neoplastic invasion each of these complications varies with the type of aneu-
Vasculitis (see Box 1-10) rysm and its location. Aneurysm expansion is governed
Noninflammatory vasculopathy (see Box 1-10) by Laplaces law (wall tension $ pressure " radius). As a
Chronic dissection rule, the larger the aneurysm, the more rapid the rate of
Congenital expansion and the greater the likelihood of rupture.
Several forms of arterial dilation may be confused
with an aneurysm:
Arterial ectasia is the age-related change that
infection, or from penetrating trauma. Infectious aneu- causes arteries to become dilated, tortuous, and
rysms are typically saccular, occur at unusual sites, lengthened (Fig. 1-17). Ectasia is particularly
and can be multiple (see Figs. 6-28 and 7-25). They are common in the thoracic aorta, abdominal aorta,
most commonly seen in the aorta, viscera, and lower and iliac and splenic arteries.
extremity arteries. In addition to bacterial infections, Arteriomegaly is the diffuse enlargement of a long
tuberculous arteritis may cause an aneurysm to form.41 arterial segment (Fig. 1-18). It is typically seen in
Traumatic pseudoaneurysms follow blunt trauma (e.g., the iliac, carotid, and femoropopliteal vessels. The
deceleration injury), criminal penetrating trauma, and underlying pathology may be elastin deficiency
medical procedures (e.g., catheterization, surgical repair) within the media.42
(see Fig. 6-21). Like infectious aneurysms, they usually Compensatory dilation of inflow arteries occurs
are saccular and eccentric and often occur in the absence in high-flow states such as arteriovenous malfor-
of other vascular disease. Other causes of aneurysms are mations and fistulas, hemodialysis grafts, and
considered in the following sections (Fig. 1-16). hypervascular tumors.
The potential complications of aneurysms and pseu- Poststenotic dilation results from turbulence beyond
doaneurysms are rupture, thrombosis, distal embolization a site of significant arterial narrowing (Fig. 1-19).
14 I. BASIC PRINCIPLES AND TECHNIQUES
BOX 1-10
M A J O R VA S C U L I T I D E S
A N D VA S C U L O P A T H I E S
Angiography shows smooth luminal narrowing, irregu- FMD most often attacks the renal arteries. Less common
lar mural plaques, or complete occlusion (Fig. 1-24). On sites include the carotid artery, external iliac, and mesen-
the other hand, human veins are relatively resistant to teric arteries.84,85 Multiple beds are involved in about
the effects of radiotherapy.82 one fourth of cases.86 Up to six distinct pathologic sub-
types have been described (see Table 10-2). The medial
fibroplasia type is the most common.83 Medial smooth
Noninflammatory Vasculopathies muscle cells are largely replaced by fibrous tissue and
Fibromuscular dysplasia (FMD) is a group of related non- extracellular matrix. These thickened segments alternate
inflammatory disorders distinguished by arterial nar- with regions of severe thinning of the media. The effect
rowing, small (and rarely large) aneurysms, and dissec- on the lumen is alternating aneurysms (larger than the
tions.83 The cause is poorly understood, but genetic, normal artery) and focal stenoses (string of beads)
hormonal, and mechanical stress factors are suggested. (Fig. 1-25). The less common forms of fibromuscular
dysplasia, such as perimedial fibroplasia and intimal fi-
broplasia, cause beading (beads smaller than the normal
artery), smooth and tapered stenosis, focal bandlike nar-
rowing, dissection, or aneurysms without stenoses (see
Figs. 10-21 and 10-22).
Marfan syndrome is an autosomal dominant disorder
that occurs in about 1 in 3000 to 5000 individuals.87 Mu-
tation in the FBN1 gene that codes for fibrillin-1 results
in structurally deficient microfibrils in the aortic media
and activation of media-destroying matrix metallopro-
teinases (MMP) by upregulated transforming growth
factorbeta (TGF-%) levels.88 The cellular structure of the
media becomes disorganized and weakened. Up to one
third of affected individuals have de novo noninherited
defects. The telltale thinning and elongation of the limbs
may be accompanied by ocular abnormalities and car-
diovascular complications. The latter are frequent and
include aneurysm or dissection of the proximal ascend-
ing aorta (sinotubular ectasia), aortic insufficiency,
mitral valve prolapse or calcification, and pulmonary
artery dilation89 (see Fig. 6-26).
FIGURE 1-24 Radiation arteritis affecting both common femoral Ehlers-Danlos syndromes are a set of rare genetic disor-
arteries in a patient who underwent radiation therapy for cervical ders of collagen production.90 The Villefranche classifi-
cancer 7 years earlier. Note absence of other vascular disease. cation has six subtypes, but considerable clinical overlap
A B C
FIGURE 1-25 Medial fibroplasia type of fibromuscular dysplasia of the distal right renal artery. A and B, Aortogram and selective right
renal arteriogram show typical string of beads appearance of distal artery (arrow). Notably, the proximal renal artery and abdominal aorta
look normal. C, Following balloon angioplasty, luminal patency is markedly improved.
1. PATHOGENESIS OF VASCULAR DISEASES 19
exists.91 The most common findings are skin hyperextensi- aneurysm rupture. SAM may be difficult to distinguish
bility, delayed wound healing, joint hypermobility, and from PAN by imaging alone; both entities can produce
spontaneous ecchymoses. However, in the rare type IV multiple bizarre aneurysms in medium-sized visceral
(vascular) subgroup, the skin is remarkably thin but joints arteries (see Fig. 11-39).
are not hyperextensible.91,92 The underlying defect is a Loeys-Dietz syndrome is a recently identified autosomal
mutation in the gene coding for type III procollagen dominant connective tissue disorder resulting from ge-
(COL3A1); as a consequence, this important structural netic defects in the genes coding for TGF-% receptors.97
protein is defective and deficient in the arterial media. The characteristic features include arterial (especially aor-
Vascular events almost always occur before age 40 and tic) aneurysms and dissections, global arterial tortuosity,
include spontaneous arterial rupture, dissections, false hypertelorism, bifid uvula, cleft lip, and congenital heart
aneurysms, carotid-cavernous fistula, and severe angio- disease. Grange syndrome is another newly described entity
graphic complications (Fig. 1-26 and see Fig. 9-29). Almost encompassing multifocal aneurysms and stenoses, bone
any artery can be affected. Intestinal and gravid uterine fragility, brachysyndactyly, and cardiac abnormalities.98
rupture are also encountered with this devastating condition.
Segmental arterial mediolysis (SAM) is a fascinating
Extrinsic Compression
disease of unknown cause that leads to destruction
of arterial medial smooth muscle cells and eventual re- The lumen of an artery can be narrowed by a variety
placement by fibrin and granulation tissue.93 Over time, of extrinsic sources, including inflammatory masses,
extension to the entire arterial wall can produce multiple tumors, hematomas or other fluid collections, musculo-
spontaneous dissections, focal dilation, aneurysms, and skeletal structures, and cutaneous compression.
arterial occlusions. It has been postulated that SAM
is related to fibromuscular dysplasia.94 The disorder
primarily affects the mesenteric arteries and less fre- ARTERIES AND VEINS
quently the cerebral, renal, and coronary circulations.95,96
A classic presentation is intraabdominal bleeding from
Neoplasms
Primary vascular tumors are exceedingly rare, and sar-
comas of the aorta, pulmonary artery, or IVC account for
most of them99-102 (see Fig. 1-13). Most tumors of the
aorta and pulmonary artery are intimal angiosarcomas
that produce large luminal masses or emboli. Mural
angiosarcomas (which typically invade contiguous struc-
tures) are less common. Most IVC tumors are leiomyosar-
comas (see Fig. 16-27). Extravascular benign and malig-
nant tumors have several possible effects on neighboring
vessels. These patterns of hypervascularity, neovascu-
larity, vascular displacement, and vascular invasion may
be seen alone or in combination.
Hypervascularity occurs because neoplasms require
abundant blood supply for significant growth. Tumors
liberate several substances, including tumor angiogenesis
factors, that induce formation of new blood vessels. These
tumor vessels are blood channels and spaces devoid of
smooth muscle cells.103-105 The angiographic hallmark of
these changes is neovascularity, which appears as bizarrely
formed small arterial branches that have alternating di-
lated and narrowed segments and an angulated course
(Fig. 1-27 and see Figs. 10-33 to 10-35). Other features of
hypervascular tumors include enlargement of the feeding
artery, an increased number of small arteries, dense con-
trast opacification of the mass (tumor blush), filling of
enlarged vascular spaces (pools or lakes), and, occasionally,
FIGURE 1-26 Saccular internal carotid artery aneurysm in a arteriovenous shunting. The classic hypervascular tumors
patient with Ehlers-Danlos syndrome. Also note a carotid-cavernous are renal cell carcinoma, hepatocellular carcinoma, chorio-
fistula (arrow). carcinoma, endocrine tumors, and leiomyosarcoma.
20 I. BASIC PRINCIPLES AND TECHNIQUES
A B
FIGURE 1-27 A, Hepatoma of the right lobe of the liver produces hypervascularity and neovascularity in the arterial phase of the hepatic
angiogram (arrow). Note displacement of branches around the large mass. B, Later phase of the angiogram shows inhomogeneous tumor stain.
Inflammatory Disorders
Every acute inflammatory process increases blood
flow to the site and causes dilation of feeding arteries,
hypervascularity, and parenchymal stain that can
mimic a hypervascular tumor (Fig. 1-30). Chronic
inflammatory masses, such as pancreatic pseudocysts,
can displace, encase, occlude, or rupture into blood
vessels (see Fig. 12-44).
Arteriovenous Communications
Development of the capillary system between arterioles
and venules occurs through capillary network, retiform,
FIGURE 1-28 Branches of the left external carotid artery are displaced and gross differentiation stages. Direct communications
around a large metastatic mass from cutaneous melanoma (arrows). between arteries and veins without an interposed capillary
network can be normal or pathologic. The distinction
between vascular malformations and vascular tumors
Vascular invasion is another consequence of some is often confusing. The modified Hamburg classification
tumors. Many solid neoplasms show little blood vessel originally devised by John Mulliken and colleagues
proliferation. Instead, they are infiltrative or scirrhous is most widely accepted and has been endorsed by the
and compress, encase, or completely occlude adjacent International Society for the Study of Vascular Anoma-
arteries or veins. Usually it is impossible to differentiate lies106,107 (Box 1-11).
these changes from those caused by an inflammatory Vascular malformations are congenital lesions composed
mass. Invasive tumors include adenocarcinomas of of dilated, thin-walled venous, arterial, or lymphatic
the intestinal tract, pancreatic adenocarcinoma, breast channels without proliferating cells.108,109 They are always
carcinoma, and most lung cancers. Vascular displacement present at birth (although often detected later in life). They
occurs during malignant growth. Some tumors primarily tend to grow slowly and continuously with the child but
1. PATHOGENESIS OF VASCULAR DISEASES 21
A B
C D
FIGURE 1-29 Right renal cell carcinoma with renal vein and inferior vena cava invasion. A, CT scan shows a heterogeneous enhancing
mass in the right kidney, with extension to the renal vein (arrow). B, Inferior vena cava invasion is also noted (arrow). C, Early phase of right
renal arteriogram shows the hypervascular mass in the upper pole of the kidney. D, Later phase shows linear threads and streaks in right
renal vein and IVC related to tumor thrombus (arrows).
A B C
FIGURE 1-30 Severe bronchiectasis causes massive hemoptysis. A, Chest radiograph shows severe bilateral upper lobe airway disease.
B, Arteriography of right intercostal-bronchial artery trunk shows marked hypervascularity in the lateral upper lobe from collateral intercostal
vessels (arrow). C, Following microsphere embolization of the intercostal segment, the hypervascularity in the hilum from the bronchial
branches themselves becomes evident (arrows).
22 I. BASIC PRINCIPLES AND TECHNIQUES
are subject to rapid expansion with injury or hormonal Venous malformations (VMs) have slightly dilated or
stresses.110 They never regress. Many are associated with nondilated inflow arteries, variable flow patterns,
an underlying clinical syndrome. Vascular malformations and large spongy venous spaces. They are the most
are most frequently located in the extremities, head, neck, common type of vascular malformation and can
and pelvis, but they may be found at almost any site in occur almost anywhere on the body.111 Multiple
the body. skin lesions on the trunk, soles, and palms are seen
with blue-rubber bleb nevus syndrome. Certain VMs
are sometimes mistakenly called hemangiomas
(e.g., adult liver hemangioma).
BOX 1-11
Capillary malformations produce the so-called port
VA S C U L A R A N O M A L I E S wine stain skin lesion.
Arteriovenous malformations (AVMs) result from
Vascular tumors failure of regression of the retiform plexus (nidus)
Hemangioma that directly connects arteries and veins in the fetus.
Kaposiform hemangioendothelioma They are distinguished by marked dilation of the
Pyogenic granuloma feeding vessels, hypervascularity, numerous arterio-
Hemangiopericytoma venous connections around the nidus, early venous
Glomuvenous malformation filling, and rapid venous washout (Fig. 1-31).
Cavernous angioma AVMs typically pass through several stages, from
Vascular malformations dormancy, to expansion with associated pulsation
Venous malformation and thrill, to destruction with pain, bleeding or
Arteriovenous malformation ulceration, to decompensation and possibly heart
Arterial malformation failure.110 Trauma, hormonal changes, and ischemia
Lymphatic malformation seem to encourage growth; the latter response is one
Capillary malformation of several reasons to avoid proximal occlusion of
Combined types feeding arteries.
A B
FIGURE 1-31 Arteriovenous malformation of the left upper arm. A, The malformation is primarily fed by the radial recurrent artery
(arrow) and branches of the deep brachial artery. B, Early and rapid venous filling occurs during the arterial phase of the angiogram.
1. PATHOGENESIS OF VASCULAR DISEASES 23
Lymphatic malformations (LMs) are categorized as Most patients are found to have mutations in the endo-
microcystic, macrocystic, or mixed. In the past, glin (ENG) or activin type-II-like receptor kinase (ALK1)
they were referred to as lymphangiomas or cystic genes that code for endothelial receptors of the TGF-%
hygromas. Most LMs are found in the head or neck, type. These proteins are intimately involved in maintain-
with the remainder occurring in the axilla, trunk, ing overall vascular integrity. A definitive diagnosis re-
or extremities.110 Many lesions have associated soft quires the presence of three of the following conditions:
tissue or skeletal overgrowth; the overlying skin is recurrent spontaneous epistaxis, multiple telangiectasias,
often marked by a bluish tinge. visceral vascular malformations, and autosomal dominant
inheritance.114
Benign vascular tumors undergo periods of cellular Arteriovenous fistulas (AVFs) are almost always ac-
proliferation and usually involute over time. They may quired direct connections between an artery and neigh-
be cutaneous or found in internal organs, including the boring vein. Most arteriovenous fistulas are caused by
brain, liver, spleen, pancreas, and kidneys (see Fig. 12-41). trauma. Color Doppler sonography or MR angiography
Capillary hemangiomas are in a growth phase; cavernous can often identify the site of communication along with
hemangiomas are in a quiescent stage and marked by nor- the enlarged feeding artery and early and rapid filling of
mal-caliber feeding vessels, large vascular channels, and the draining vein (Fig. 1-34; see Figs. 7-12 and 10-31).
early filling of vascular spaces that persists through the AVFs can close spontaneously or enlarge over time.
venous phase of a contrast imaging study (Fig. 1-32). Patients often are asymptomatic but may present with
Telangiectasias are focal lesions composed of dilated ar- local symptoms, distal ischemia (from a steal phenome-
terioles, capillaries, and venules. They are typically found non), or high-output heart failure. Very rarely, fistulas
on the skin and mucous membranes but can be seen also are congenital.115
in visceral organs. Hereditary hemorrhagic telangiectasia Arteriovenous shunts are normally present in many
(HHT, once called Osler-Weber-Rendu syndrome) is an auto- vascular beds. These physiologic shunts sometimes be-
somal dominant disorder in which telangiectasias are come quite prominent116 (Fig. 1-35). They may be seen
present on the lips and mouth and in the intestinal tract, also in certain disease states, such as cirrhosis and in
liver, spleen, lung, and brain112,113 (Fig. 1-33; see Fig. 11-36). hypervascular tumors (Fig. 1-36).
A B
FIGURE 1-34 A, Arteriovenous fistula between the superficial femoral artery and vein after femoral artery catheterization. Note the
marked enlargement of the left iliac arteries compared with the right side. B, Selective injection in the left common femoral artery in oblique
projection identifies the site of communication.
Vascular Injury
Arteries and veins can be damaged in many ways.117
FIGURE 1-35 Prominent arteriovenous shunts after balloon Penetrating injuries may be caused by sharp objects,
angioplasty of the superficial femoral artery in a patient with gunshot wounds, bone fragments, or medical proce-
peripheral vascular disease. dures. Gunshot wounds produce vascular injury by
1. PATHOGENESIS OF VASCULAR DISEASES 25
VEINS
A B C
FIGURE 1-39 Venacavography reveals inflow defects from unopacified blood from both moieties of a circumaortic left renal vein (arrows).
The hallmark of this finding is change over the course of the injection (B and C).
1. PATHOGENESIS OF VASCULAR DISEASES 27
vein wall remains thickened and scarred, minimally Chronic Venous Diseases
compliant, and associated with valve damage.
Chronic disorders of the veins are typically divided into
Pulmonary embolism is the most feared compli-
primary (no discernable reason for vein dysfunction)
cation of systemic DVT. The reported frequency is
and secondary forms (which by definition follows some
10%.126 Since the groundbreaking study of Barritt
acute venous event.) Primary chronic venous insufficiency
and Jordan in 1960,127 numerous studies have
(CVI) is predicated on some type of valve dysfunction,
proven that therapeutic anticoagulation of suffi-
often involves venous reflux but not venous obstruc-
cient duration will reduce the risk significantly.
tion. The spectrum ranges from telangiectasias and
Chronic occlusion, vein/valve injury, and/or
varicose veins (which afflict about 20% of the general
associated venous reflux (Fig. 1-40). Even though
population) to active ulceration (#1%). Despite centu-
most venous segments will recanalize after acute
ries of study, the exact etiology of varicose veins is still
DVT, some valve damage is the rule. The major late
obscure.128,129 The unifying feature is valve dysfunction
sequelae from valvular damage with or without
and incompetence which develops at multiple sites
persistent obstruction is the post-thrombotic syndrome,
over a short time.130 The pathologic abnormalities are
which is characterized by limb swelling, hyperpig-
well described (intimal thickening, mural fibrosis, elas-
mentation, and venous ulcers. Although more
tic fiber atrophy, poor contractility and compliance.)
than half of patients with VTE may suffer mild forms
Whether these findings are primary or secondary is not
of this vexing problem, severe symptoms develop
established.
in fewer than one fourth of cases.121 The major
Secondary CVI is characterized by venous hyperten-
predictors of post-thrombotic syndrome are the rate
sion with ambulation.130 The disorder may be the result
of clot resolution, recurrence of thrombosis, and the
of reflux alone from valves damaged by prior throm-
extent and distribution of reflux and obstruction.
bosis or reflux combined with chronic venous obstruc-
Rarely, malignancies invade neighboring veins and tion. The major determinants of venous pressure are
produce tumor thrombus that mimics bland clot (see reflux (caused by abnormal vein valves), venous ob-
Fig. 1-29). The most susceptible veins are the portal, struction, and failure of the calf pump (a function of
renal, and hepatic veins and the IVC. central vein patency, abnormal joint or muscle activity,
and valve failure). This secondary form of valve incom-
petence (about four times less common than the pri-
mary form) may occur after an episode of acute venous
thrombosis. Malfunction of the perforating veins (from
primary valve incompetence or reflux from deep vein
occlusion) between the superficial and deep systems is
critical. Elevated pressure is transmitted to superficial
veins, which leads to distended skin capillaries and
transfer of fluid, macromolecules, and red blood cells
to the interstitium.130 A cycle of chronic inflammation is
set in motion.
In most countries, CVI is one of the most common
chronic disabling conditions in the population. It is
more often seen in women (especially after multiple
births), in older or obese patients, and in individuals
with family history. The American Venous Forum has
created a classification system for chronic venous dis-
eases (CEAP) that denotes clinical class, etiology, ana-
tomic location of obstruction and reflux, and pathology
(reflux vs. obstruction).131 From this scheme, disease is
divided among seven grades (class 0, absent signs;
class 1, telangiectasias; to class 6, active venous limb
ulcers).
Neointimal Hyperplasia
Neointimal hyperplasia is the reaction of veins to acute
FIGURE 1-40 Chronic superior vena cava occlusion with injury or chronic hemodynamic changes. Clinically, the
well-developed collateral circulation. disease is seen most often in venous bypass grafts and
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58. Canyigit M, Peynircioglu B, Hazirolan T, et al. Imaging characteris- dysplasia of the visceral arteries. Am J Gastroenterol 1996;91:1635.
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59. Cid MC, Garcia-Martinez A, Lozano E, et al. Five clinical dysplasia with multiorgan failure. Arch Intern Med 1996;156:2611.
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Clin North Am 2007;33:819. drome. Circulation 2008;117:2802.
60. Wang X, Hu Z-P, Lu W, et al. Giant cell arteritis. Rheumatol Int 88. Matt P, Habashi J, Carrel T, et al. Recent advances in understand-
2008;29:1. ing Marfan syndrome: should we now treat surgical patients with
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96. Ryan JM, Suhocki PV, Smith TP. Coil embolization of segmental cating occlusive atherosclerotic peripheral vascular disease. Clin
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C H A P T E R
2
Patient Evaluation and Care
Karim Valji
In 1967, Dr. Alexander Margulis proposed a new subspe- (in time and space) from the interventional suite as possi-
cialty within the family of imaging sciences which he ble. The goals of the interview and examination are to es-
called interventional radiology.1 For some time thereaf- tablish rapport, review the history firsthand, explain the
ter, interventional radiologists (IRs) were consultants who procedure in detail (and thus obtain informed consent), and
performed minimally invasive angiographic procedures reduce anxiety. Family and significant others are encour-
(at the request of clinicians) with little or no responsibility aged to participate in the discussion. Ideally, inpatients are
for patient care before or after. This practice model has assessed the day before the case is scheduled. Outpatients
been transformed over the past 40 years. Interventionalists are evaluated in a clinic or office dedicated to this work,
(including the many subspecialists from other fields who where support staff (trainees, nurses, physician extenders,
also do this work) now assume full clinical responsibility and administrative assistants) are fully engaged in IR.2
for their patientsthey are true clinicians. As such, IRs
are obligated to conduct the initial patient assessment,
determine the best course of therapy, and provide long-
History and Physical Examination
term care and management after the procedure is com- The clinical evaluation includes several components
pleted. Experienced interventionalists will agree that a (Box 2-1). The physician must be confident that there are
successful and safe technical outcome depends as much appropriate indications for the proposed intervention
on preprocedure and postprocedure care as it does on based on best practice criteria established in the med-
performing the case itself. The concepts set down in this ical literature or endorsement by the Society of Interven-
chapter form the cornerstone of modern interventional tional Radiology (SIR) and the Cardiovascular and Inter-
radiology practice. The details and nuances may vary ventional Radiology Society of Europe (CIRSE).3 Risk
among institutions, but the principles are universal. factors that may require a delay or modification of the
proposed procedure or an alternative therapy are sought
(Boxes 2-2 and 2-3). A focused physical examination is
PREPROCEDURE CARE performed, but it is prudent to assess the airway, lungs,
heart, and abdomen in almost all patients. For angio-
graphic procedures, the interventionalist should evalu-
Patient Referral and Contact
ate and document the following parameters:
For simple diagnostic and interventional procedures (e.g.,
Proposed puncture site (contraindications include,
vascular access placement), patient referral without direct
for example, groin infection, common femoral
contact between physicians is appropriate. For more
artery aneurysm, overlying hernia, fresh incision,
complex or controversial clinical problems, a discussion
recent injury)
between the interventionalist and the referring physician
All extremity pulses, using a Doppler ultrasound
ensures that the appropriate procedure is done, the potential
probe when necessary
risks for the individual patient are appreciated by every-
Status of extremities (e.g., color, perfusion,
one involved, and the likely outcome is understood.
presence of swelling, ulceration)
The interventionalist should review the medical history
and all pertinent diagnostic tests and imaging studies before Thrombophilic (hypercoagulable) states are an im-
seeing the patient. With this approach, one can avoid portant risk factor for vascular thrombosis and can be
raising the specter of an intervention that is ultimately not associated with significant complications from diag-
indicated. The initial conversation between patient and nostic and therapeutic vascular procedures.4-6 The ma-
physician is vitally important and should occur as far away jor hereditary and acquired disorders are listed in
32
2. PATIENT EVALUATION AND CARE 33
E VA L U A T I O N O F T H E P R I M A RY R I S K FA C T O R S
PAT I E N T F O R C O N T R A S T- I N D U C E D
N E P H R O PAT H Y
History of current problem
Pertinent medical and surgical history Preexisting renal dysfunction (serum creatinine
Review of organ systems !1.2-1.5 mg/dL, 106-132 mmol/L)
Cardiac Diabetes
Pulmonary Dehydration
Renal Hypotension
Hepatic Congestive heart failure
Hematologic (e.g., coagulopathy, thrombophilic Large contrast dose
state) Advanced age
Endocrine (e.g., diabetes) Anemia (hematocrit "40%)
History of allergies or adverse reactions to Nephrotoxic drugs
sedatives/anesthetics
Current medications (including prescribed/illicit
narcotics or sedatives)
Directed physical examination
Weight
BOX 2-4
Airway
Heart and lungs AMERICAN SOCIETY
OF ANESTHESIOLOGY
P H Y S I C A L S TAT U S
C L A S S I F I C AT I O N S C H E M E
Administration of
Contrast agents, including allergic reactions
BOX 2-5
and nephrotoxicity
C O N D I T I O N S T H A T M AY Sedatives and analgesics (e.g., respiratory
REQU IRE MONITORED/ depression, hypotension)
GENERAL ANESTHESIA Other medications that may be required during
or after the procedure (e.g., allergic reaction,
Young age (children) bleeding from anticoagulants)
Advanced age Radiation injury from prolonged fluoroscopic
Morbid obesity procedures
Potential airway compromise (e.g., history of sleep The particular risks for specific diagnostic and inter-
apnea) ventional procedures are discussed in later chapters. As a
Chronic narcotic use or abuse rough guide, the overall incidence of major complications
Severe heart, lung, or liver disease (Box 2-6) should be no more than 1% to 2% for the more
Increased risk of aspiration common interventions (e.g., vascular access placement,
Very painful or prolonged procedures (e.g., biliary inferior vena cava filter placement, percutaneous biopsy
tract dilation) and drainage procedures, dialysis access interventions).10-12
Patient inability to cooperate However, older patients and those with established risk
factors are more likely to suffer a bad outcome such
as bleeding, infection, thrombosis, renal dysfunction, or
allergic reactions to administered drugs.13
the United States, the implied consent doctrine is con- In addition to having the patient (or legal representa-
sidered to be in force with any medical procedure in tive) sign a consent form, a preprocedure note stating
which a delay could lead to severe disability, severe pain, that informed consent was obtained must be placed in
or death. In this rare situation, consent is unnecessary if the medical record before starting the case. Some practi-
the patient cannot give his or her own approval and no tioners list both common and serious (but rare) risks, but
legal representative is immediately available.9 others prefer to be less specific. The thrust of the conver-
To give informed consent, the patient must under- sation and patient queries should be documented. The
stand the need for undergoing the procedure, potential preprocedure note also includes a brief medical history,
risks and expected immediate and long-term outcomes, the specific indications for the procedure, directed phys-
the consequences of refusing the intervention, and the ical examination, and results of relevant imaging and
nature of alternative studies or therapies. To avoid ex- laboratory tests.
ceeding consent, the discussion should include conceiv-
able interventions (e.g., thrombolysis, angioplasty, or
stent placement in a patient undergoing angiography for
evaluation of peripheral vascular disease).
Informed consent is both a legal and medical con- BOX 2-6
cept. In the United States, some states have adopted a
prudent patient standard that is based on the infor- SOCIETY OF
mation an average patient needs to make a decision I N T E RV E N T I O N A L
regarding medical care. Other states use a standard RADIOLOGY DEFINITIONS
based on the information that a prudent physician OF ADVERSE EVENTS
in the community would have discussed for such a
procedure. The interventionalist should explain the Minor Complications
various elements of the intervention that could result No therapy, no consequence
in an untoward event: Nominal therapy, no consequence; includes over-
night admission for observation only
Access, including the possibility of local infection,
bleeding, or hematoma formation (and pseudoan- Major Complications
eurysm, arteriovenous fistula, thrombosis or
dissection with arteriography) Require therapy, minor hospitalization (#48 hr)
Needle, catheter, or guidewire manipulation en Require major therapy, unplanned increase in level
route to and at the intended site of angiography of care, prolonged hospitalization (!48 hr)
or intervention (e.g., risk of bleeding, organ Permanent adverse sequelae
injury, dissection, vessel perforation or thrombo- Death
sis, nerve damage, arrhythmias, stroke)
2. PATIENT EVALUATION AND CARE 35
Laboratory Testing
Until recently, gadolinium-based contrast agents
The purpose of preprocedure laboratory testing is to were favored as a safe alternative to iodinated materials
minimize risk by detecting (and when feasible correct- during intravascular interventions in patients with
ing) relevant abnormalities, altering the technique as baseline renal insufficiency. Some of these agents pose a
needed, or canceling the case and choosing a safer treat- risk (albeit very small) for causing nephrogenic systemic
ment. Preprocedure studies may be routine (screening) or fibrosis in individuals with preexisting severe chronic or
selective (directed).14 Indiscriminate testing has proved to acute renal insufficiency (eGFR "30 mL/min.). This
be of little value in virtually every medical and surgical rare disorder is characterized by widespread and often
study ever published.15-17 However, selective testing is debilitating dermal (and sometimes visceral organ)
warranted before vascular and interventional proce- sclerosis.20,21 As such, gadolinium-based agents are no
dures. Screening is generally unnecessary in otherwise longer used during vascular procedures unless renal
healthy patients younger than 40 years of age. Testing is function is essentially normal.
certainly advisable in older adults and those with pre-
disposing risk factors. The acceptable interval between Coagulation Parameters
test result and procedure varies among hospitals and Significant bleeding from interventional procedures is
clinical situations and cannot be generalized. uncommon. It is an axiom in interventional radiology
(IR) that the individual risk is largely a function of the
Renal Function coagulation status of the patient (Box 2-7), the likeli-
Serum creatinine is still widely used as a proxy for kid- hood of traversing a major artery or vein, and the ability
ney function, but it is an imprecise measure of such. Es- to detect and then manually control bleeding when it
timated glomerular filtration rate (eGFR) is a more accu- occurs. In fact, there are equivocal data regarding the
rate indicator of renal insufficiency. Contrast-induced value of coagulation screening tests in predicting the
nephropathy (CIN) is marked by a significant rise in likelihood of bleeding from invasive procedures.22,23
serum creatinine level (0.5 mg/dL or 25% of baseline) Nonetheless, routine screening for coagulopathy is the
1 to 3 days after intravascular administration and by practice in many institutions based on tradition and
resolution at 7 to 10 days. This (usually) transient dys- sometimes stated policy. A more judicious approach is
function is related to direct toxic effects on the kidney by favored by some practitioners:
oxygen free radicals or ischemia of the renal medulla.18 In
For diagnostic and most therapeutic vascular
the general population and in patients with eGFR greater
procedures, individuals with known or suspected
than 60 mL/min (stage 1 or 2 chronic kidney disease), the
risk factors for bleeding should be tested (see
overall risk of CIN after diagnostic angiography is low
Box 2-7).
("2%). The risk increases to about 5% in patients with
With thrombolytic therapy or endovascular inter-
preexisting mild renal dysfunction and 33% or greater
ventions that may require parenteral antithrombin
in patients with diabetes and severe renal insufficiency
(eGFR "30 mL/min, stage 4 or 5 chronic kidney dis-
ease).19 Only a small fraction of patients who suffer this
complication require long-term hemodialysis. However,
some experts believe concerns about CIN are exagger- BOX 2-7
ated and that use of iodinated contrast should not be
avoided in patients with moderate renal dysfunction.19 R I S K FA C T O R S F O R
The traditional approach to preventing CIN is hydra- BLEEDING FROM
tion with intravenous (IV) saline (1 to 1.5 mL/kg/hr) for VA S C U L A R A N D
6 to 12 hours before and at least several hours after intra- I N T E RV E N T I O N A L
vascular contrast administration. In addition, several PROCEDURES
other measures should be considered when the risk is
Thrombocytopenia
increased:
Anticoagulant medications
The total volume of contrast agent is strictly Liver disease
limited. Contrast material is diluted as much as History of bleeding diathesis
possible without compromising diagnostic quality. Malignant hypertension
The lowest osmolality agent is used. Malnutrition
Carbon dioxide may replace or supplement Hematologic malignancy
standard iodinated contrast in some situations Splenomegaly
(see Chapter 3). Disseminated intravascular coagulation
Selected chemotherapeutic agents
Several pharmacologic regimens may reduce the like-
lihood of CIN (see discussion below).
36 I. BASIC PRINCIPLES AND TECHNIQUES
or antiplatelet agents, the substantial risk of local clear liquids within 6 hours and are given nothing by
or remote bleeding supports routine testing. mouth (NPO) within 2 hours of the expected start time
Many nonvascular interventional procedures (e.g., to prevent aspiration from vomiting caused by contrast
deep large-core biopsy or fluid drainage, nephros- agents, sedatives, or individual patient factors.27 For
tomy, biliary drainage) can result in hemorrhage inpatients who will receive significant volumes of intra-
that is only apparent after substantial blood loss vascular contrast, overnight IV hydration should be
and is often difficult to control; thus, testing is done considered when feasible. Outpatients are encouraged
routinely. Other procedures (e.g., small-gauge to drink plenty of fluids. IV fluids should be ordered in
superficial biopsy) do not require screening tests. consultation with the referring physician for patients
with cardiac or renal disease.
Commonly performed coagulation tests are out-
lined in Box 2-8. Thresholds for defining a coagulopa- Medications
thy and measures for correcting them22-25 are outlined Patients are instructed to take their regular medications
in Tables 2-1 and 2-2. Based on limited but promising (particularly cardiac, respiratory, and antihypertensive
experience using more relaxed parameters for tun- drugs) with a few sips of water on the day of the proce-
neled central venous catheter placement, some practi- dure, with certain exceptions:
tioners insert such devices when the INR is less than
2.0 or the platelet count is greater than 25,000/dL.26 Insulin-dependent diabetic patients may inject
their usual insulin doses for early morning
Patient Preparation cases or reduce their morning dose by one half
for midday cases to avoid hypoglycemia.
Diet and Hydration Noninsulin-dependent diabetics may
When moderate sedation is planned, oral intake or withhold drugs until after the procedure.28
gastrostomy feeding restrictions must comply with in- Blood glucose monitoring is advisable during
stitutional guidelines. Typically, patients are limited to the case.
IV, intravenously.
2. PATIENT EVALUATION AND CARE 37
Diabetic patients with preexisting renal dysfunc- LMW heparin compounds (e.g., enoxaparin
tion who take the oral hypoglycemic metformin [Lovenox]) will generally not alter standard
(Glucophage) are at a very small risk for severe coagulation tests. Studies in coronary interven-
(and sometimes fatal) lactic acidosis resulting tions have failed to show a significant added risk
from metformin accumulation if CIN occurs after of bleeding when these agents are administered.33
an angiographic procedure.29 In these individuals, However, there is a paucity of published data
metformin is withheld for 48 hours before elective on their impact during noncoronary interven-
cases, at the time of the procedure for urgent tions. It is wise to hold doses for 24 hours before
cases, and 48 hours afterward.30 The drug may be elective cases.
resumed after obtaining a new serum creatinine. Most practitioners favor discontinuation of
Heparin is stopped 2 to 4 hours (depending on aspirin or clopidogrel (Plavix) about 7 to 10 days
the most recent partial thromboplastin time [PTT] before elective, high-risk procedures. This step
value) before most interventional procedures and is not necessary for lower risk procedures, such
restarted several hours later. as tunneled central venous catheter insertion.
Warfarin therapy complicates many IR proce- However, if the agents were given in conjunction
dures. The drug is usually withheld for 3 to with bare or drug-eluting coronary stents, they
5 days before elective cases. Often, a low molecu- should not be discontinued without the consent
lar weight (LMW) or unfractionated heparin of a cardiologist.31
bridge is necessary to protect the patient from Preprocedure sedation (e.g., lorazepam [Ativan],
a thrombotic or embolic event31,32 (Box 2-9). If the 0.5 to 2.0 mg orally) is favored by some interven-
PT or INR is mildly elevated on the day of the tionalists.
study, infusion of fresh frozen plasma should be
considered. Contrast Reaction Pretreatment
Severe allergic reactions follow less than 1 in 10,000 doses
of the most commonly used intravascular nonionic isos-
molar contrast materials.34,35 The value of universal pre-
BOX 2-9 treatment of patients with a history of a prior contrast
material reaction is being questioned. Nonetheless, it
I N D I C AT I O N S A N D remains accepted practice in many institutions to pre-
PROTOCOL FOR medicate patients with a history of moderate to severe
A N T I C O A G U L AT I O N contrast allergy before giving these drugs. Even with pre-
BRIDGE AFTER treatment, so-called breakthrough reactions do occur.36
W I T H H O L D I N G WA R F A R I N A variety of protocols are acceptable, but all include a
corticosteroid taken at least 12 hours beforehand.35,37
Prosthetic heart valve (most cases) There is no evidence that oral or IV steroids are of
VTE within 1 year any benefit when given immediately before contrast is
Severe thrombophilia injected.37 Accepted regimens include:
Active cancer
Atrial fibrillation with history of stroke/TIA and Corticosteroid: 32 mg methylprednisolone
additional risk factor (Medrol) orally or 50 mg prednisone orally
Recurrent VTE 12 hours, 7 hours (optional), and 2 hours
before the procedure (mandatory)
Day !5 Stop warfarin
Histamine (H1) receptor blocker: 25 to 50 mg
Day !3 Start LMWH
diphenhydramine (Benadryl) orally 1 to 2 hours
Day !1 Check INR, hold LMWH after morning dose
before the procedure (optional)
Day 0 Stop unfractionated heparin 4 hours before
(if prescribed)
Prevention of Contrast-Induced Nephropathy
Day "1 Restart LMWH and warfarin
N-acetylcysteine (NAC, Mucomyst) is an antioxidant that
Adapted from Vinik R, Wanner N, Pendleton RC: Periproce- behaves as a scavenger of oxygen free radicals and in-
dural antithrombotic management: a review of the literature hibitor of certain proteins implicated in kidney damage
and practical approach for the hospitalist physician. J Hosp Med
2009;4:551.
from iodine-based contrast media. Even though results
INR, International Normalized Ratio; LMWH, low molecular of clinical trials have been mixed, the preponderance
weight heparin; TIA, transient ischemic attack; VTE, venous of evidence suggests that NAC is indeed more renal
thromboembolic disease.
protective than IV hydration alone in patients with
underlying renal insufficiency.38-42 Dosing protocols
38 I. BASIC PRINCIPLES AND TECHNIQUES
INTRAPROCEDURE CARE
Infectious Disease Precautions
The risk for transmission of blood-borne pathogens from
Time Out
physician to patient during interventional cases is vanish-
Immediately before starting any interventional or ingly small. However, the risk for transmission from pa-
surgical procedure, and with the entire operating team tient to operator is very real.61-63 In particular, infection
present, The Joint Commission mandates a time out with hepatitis B or C virus and human immunodeficiency
or shout out.53 Identity is established by announcing virus (HIV) is of particular concern to health care workers.
the name, medical record number, and birthdate on Because of the potentially grave consequences of these
the patients wrist band. The impending procedure is infections, Universal Precautions should be followed,
verbalized along with the site and side of intervention as mandated in the United States by the Occupational
(e.g., intraarterial embolization of the right kidney). Safety and Health Administration. These measures include
The signed consent form is reconciled with the clinically use of surgical gowns, masks, protective eyewear, and two
indicated intervention. The on-site existence of any pairs of gloves. Gloves should be changed every few hours
specialized equipment necessary for the procedure is during long procedures and whenever glove integrity is
confirmed. Finally, any known drug allergies are stated. breached.64 A secure place for all sharp objects is kept on
the interventional table (Online video 3-1). Needles are
never recapped with a gloved hand alone. If a needle stick
Radiation Safety
does occur, the occupational safety department should be
The radiation dose to the patient can be minimized consulted immediately.
by limiting fluoroscopy time and the number of digital
acquisitions, using the lowest imaging frame rates
necessary to obtain diagnostic information during fluo-
Patient Monitoring
roscopy, careful beam collimation, and use of lead The interventionalist should note the baseline vital signs
shields (including gonadal protection when appropri- before the procedure begins. The patient undergoes con-
ate). Some complex or prolonged IR cases lead to sig- tinuous monitoring of electrocardiogram, respiratory
nificant radiation exposure and a real risk for radiation rate, end tidal carbon dioxide, and oxygen saturation
dermatitis.54-57 Transient skin injury may occur after a (by pulse oximetry). Automated cuff blood pressure
dose of 2 Gy. Permanent damage usually requires doses measurement is obtained every 5 to 10 minutes, depend-
greater than 5 Gy. The procedures with greatest overall ing on the patients condition. The nurse records these
risk include transjugular intrahepatic portosystemic factors, the degree of sedation, and overall patient status
shunt, embolization, and intravascular stent placement every 5 to 10 minutes throughout the case. Oxygen is
in the abdomen or pelvis. given by nasal cannula or face mask to maintain the oxy-
Therefore, a measure of radiation exposure should be gen saturation above 90% to 92%.
included in the dictated report for all IR procedures.
Fluoroscopy time is a relatively poor proxy for dose and
associated radiation risk. Peak skin dose (PSD), air
Fluid Management
kerma (in mGy), and dose area product (DAP, in Gycm2) The type and rate of IV fluid infusion are based on pre-
are more accurate indicators.58 Doses should be carefully existing conditions (e.g., diabetes, renal failure, congestive
monitored for the higher risk cases or when multiple heart failure) and the volume of intravascular contrast
sequential procedures are performed. material being given. As a general rule, fluids are run at
Interventionalists are at particular risk for excessive about 1 mL/kg/hr. One study found that the incidence of
radiation exposure over their lifetimes.59,60 The major renal dysfunction after angiography was lower with vig-
complications of long-term radiation exposure in these orous saline hydration alone than with the use of mannitol
providers include cataracts, certain solid organ cancers, or furosemide to induce diuresis after the procedure.65 A
and hematologic malignancies. Personal radiation moni- Foley catheter is placed when angiographic imaging over
toring badges must be worn at all times. Operators should the pelvis is required and for patient comfort and monitor-
protect themselves by wearing protective clothing, such ing of urine output during long or complex interventions.
as body aprons, thyroid wraps, and leaded glasses. Inter-
ventionalists should be diligent about using careful beam
collimation, last image hold, and moveable leaded barriers
Sedation and Analgesia
during fluoroscopy and manual acquisition of digital Patients undergoing interventional radiologic proce-
images. Finally, appropriate tube angulation can greatly dures always experience some anxiety and pain, but
reduce radiation exposure to the arm during nonvascular the degree of discomfort may not reflect the invasive-
procedures and dialysis access interventions. ness of the intervention. Perhaps the most important
40 I. BASIC PRINCIPLES AND TECHNIQUES
(and sometimes undervalued) measure to reduce anxi- fentanyl and midazolam. The interventional nurse must
ety and pain is reassurance. Patients can tolerate an in- work closely with the interventionalist to achieve a
vasive procedure more easily when the operator and steady but safe level of sedation and analgesia until the
other personnel show genuine concern for the patients case is finished.
fears and discomfort and alert him or her to each sensa- The chief signs of overmedication are a drop in
tion about to be felt as the case proceeds. oxygen saturation and respiratory depression. Some
The goals of sedation during interventional proce- patients display a delayed or hypersensitive reaction
dures are relief of pain, anxiolysis, partial amnesia, and to even small doses of these medications. Oxygen
control of patient behavior. In most cases, these goals administered by nasal cannula or face mask is given
can be met with moderate (conscious) sedation, in which if the oxygen saturation falls below 90%.
the individual is calm, drowsy, and may even close his Pediatric sedation is the subject of numerous reviews.69
or her eyes but is responsive to verbal commands and
able to protect his reflexes and airway.66,67 Deep sedation
Treatment of Adverse Events and Reactions
(in which protective reflexes are lost) and general anesthe-
sia are required for some cases but should be adminis- Adverse events are relatively infrequent during inter-
tered only by an anesthesiologist or other provider spe- ventional procedures. Successful management depends
cially trained in these techniques. on recognizing problems quickly, acting promptly, and
The standard analgesic and sedative agents employed employing basic resuscitative efforts:
in IR are narcotics, benzodiazepines, and neuroleptic
Continuous patient monitoring
tranquilizers. A wide variety of drugs can be used to
Protecting the patients airway
produce moderate sedation. One of the most popular
Securing the intravenous line and administering
combinations is midazolam and fentanyl.67,68
fluids as needed
Midazolam (Versed) is a short-acting intravenous benzo-
Giving supplemental oxygen
diazepine that acts on GABA receptors to cause central
Calling for assistance early
nervous system depression (including anxiolysis and ante-
grade amnesia). It is metabolized by the liver. The onset of Some of the more common clinical scenarios are outlined
action is 2 to 4 minutes, and the duration of effect is about in Boxes 2-11 through 2-14.
45 to 60 minutes.66 The standard initial dose is 0.5 to 1.0 mg
IV. Additional boluses are given every 3 to 5 minutes to Reaction to Sedatives and Analgesics
achieve the desired level of sedation. The optimal dose The most common symptoms of overdose are hypoxia,
often is lower in patients with small body mass, advanced respiratory depression, and unresponsiveness. Less com-
age, liver or cardiopulmonary disease, baseline hypoten- monly, patients exhibit nausea, vomiting, hypotension,
sion, or a depressed level of consciousness. The major side bradycardia, agitation, or confusion. Hypoxia alone usu-
effects of midazolam are respiratory depression and apnea. ally resolves with supplemental oxygen, a neck tilt or jaw
Fentanyl (Sublimaze) is a short-acting narcotic opioid thrust to maintain the airway, and withholding additional
analgesic that also is metabolized by the liver. Its onset sedatives. Nausea and vomiting respond to a variety
of intravenous action is 2 to 4 minutes, and the duration of antiemetic agents, including 2.5 to 10 mg IV of the dopa-
of effect is about 30 to 60 minutes.66 The initial and incre- mine antagonist prochlorperazine (Compazine) or the sero-
mental IV dose is 25 to 50 $g. Relatively large amounts tonin 5-HT3 blocker ondansetron (Zofran), 4 mg IV.
may be required in patients with a history of chronic
narcotic use or abuse. Major side effects include nausea,
pruritus, dysphoria, and respiratory depression.
After the initial administration, additional doses are BOX 2-11
generally required every 3 to 10 minutes to maintain a
continuous level of comfort. If an acceptable response to
C AU S E S O F
sedatives and analgesics is not observed before the case
INTRAPROCEDURAL
starts, the patient may not tolerate the more painful and
HYPOTENSION
prolonged interventions that may follow. In this unusual
Overmedication with sedatives/analgesics
circumstance, it may be wise to request the assistance of
Bleeding
an anesthetist or terminate the procedure. Sometimes a
Sepsis
patient does not exhibit the expected response to stan-
Contrast or drug reaction
dard dosages of these drugs. Addition of other synergis-
Myocardial infarction
tic IV agents (e.g., hydromorphone [Dilaudid] 1 to 2 mg IV
Pulmonary embolism (including air embolism)
and diphenhydramine [Benadryl] 25 to 50 mg) may be safer
and more effective than relying on escalating amounts of
2. PATIENT EVALUATION AND CARE 41
Hypertension
The most common causes of hypertension during inter-
BOX 2-13
ventional procedures are uncontrolled baseline hyperten-
C AU S E S O F sion, failure to take routine antihypertensive medications,
INTRAPROCEDURAL anxiety or pain, bladder distention, and hypoxia. Many
A LT E R E D M E N T A L S T A T U S patients become normotensive after sedatives and analge-
sics are given. The major risks of sustained hypertension
Sedative/analgesic medication are local bleeding after removal of an angiographic cathe-
Hypoglycemia ter or remote bleeding in patients undergoing treatment
Anxiety with anticoagulants or fibrinolytic agents. If severe hyper-
Hypoxia tension persists, several drugs should be considered.71,72
Vasovagal reaction Labetalol is a selective alpha-1 and nonselective beta
Bleeding/hypovolemia adrenergic blocking agent and potent antihypertensive
Myocardial infarction or dysrhythmia drug. A 20-mg IV dose is injected over 2 minutes. The
Stroke dosage may be doubled again every 10 minutes to a total
of 300 mg. The action is rapid (5 to 10 minutes) and pro-
longed (3 to 6 hours). Labetalol should be avoided in
patients with asthma or congestive heart failure.
Enalaprilat is an angiotensin-converting enzyme
BOX 2-14 (ACE) inhibitor that is quite effective for peripro-
cedural hypertension. The usual dosage is 1.25 mg IV
C AU S E S O F given over 5 minutes and again at 6 hours if necessary.
INTRAPROCEDURAL Sublingual nifedipine was once considered a first line
RIGORS agent in this setting. The drug has fallen out of favor be-
cause of scattered reports of life-threatening hypotension
Contrast or drug reaction and dysrhythmias. The newer calcium channel blocker
Sepsis/bacteremia clevidipine (1 to 2 mg IV per hour) is a better alternative.
Hydralazine 5 to 10 mg by slow IV push (and repeated
after 20 to 30 minutes) is a good backup antihyperten-
sive drug.
Patients with profound or prolonged respiratory Oral clonidine (initial dose 0.1 to 0.2 mg) may be useful
depression or hypotension should receive supplemen- in the postprocedure period.
tal oxygen, airway maintenance, and antagonists to
the offending drugs. Naloxone (Narcan) is an opiate Bleeding
antagonist. The initial dose of 0.2 to 0.4 mg given by IV When tachycardia and hypotension occur without other
push may be repeated every 1 to 2 minutes. Flumazenil explanation or the patient complains of unexpectedly
(Romazicon) is a benzodiazepine antagonist. The initial severe pain along the route of intervention, occult hem-
dose of 0.2 mg given by IV push may be repeated orrhage may be present. In this situation, bleeding will
42 I. BASIC PRINCIPLES AND TECHNIQUES
be undetectable by observation alone. Rapid infusion of to 10% dextrose is started and the blood glucose level
fluid should be started; a blood count, coagulation checked or rechecked. If symptoms are severe or the
screen, and type and cross should be obtained; and im- serum glucose level is dangerously low, one ampule
aging assessment of potentially damaged structures (50 mL) of 50% dextrose given by IV push is necessary.
should be considered.
Dysrhythmias
Mild Contrast Agent Reaction Cardiac dysrhythmias that occur during IR procedures
Patient reassurance is crucial in the management of all often are caused by guidewire or catheter manipulation
contrast reactions, regardless of severity.73,74 Symptoms in the heart, by metabolic abnormalities (such as
of a mild contrast reaction are myriad but commonly in- hypoxia, hypercarbia, or electrolyte imbalances), or by
clude urticaria, nausea and vomiting, cough, mild shak- myocardial ischemia. Mechanically induced dysrhyth-
ing, sweats, and anxiety.37 Hives usually require no spe- mias usually revert after repositioning the guidewire.
cific treatment. If itching is bothersome or the rash is Sustained dysrhythmias should be treated in consulta-
widespread, treatment with diphenhydramine (Benadryl) tion with a cardiologist or physician with experience in
(25 to 50 mg IV) is helpful. Persistent symptoms may be such situations.
addressed with an intravenous antiemetic, such as pro- Supraventricular tachycardias (!150 beats/minute)
chlorperazine 2.5 to 10 mg or droperidol 0.625 to 1.25 mg. appear as regular, narrow QRS ("0.12 sec) complexes on
an electrocardiogram. Some resolve with a chest thump
Moderate Contrast Agent Reaction or vagal action (e.g., energetic cough or Valsalva maneu-
Moderate reactions to contrast are manifested by mild ver). If not, the first line treatment in asymptomatic pa-
bronchospasm or wheezing, mild facial or laryngeal tients is an IV bolus of adenosine, which slows the sinus
edema, tachycardia (or bradycardia), and hypertension or rate and atrioventricular node conduction velocity.75,76
hypotension.37 Patients receiving beta-adrenergic blocking The initial dose is 6 mg given by rapid IV push; a 12-mg
agents may not become tachycardiac. Bronchospasm is dose may be required if there is no response after several
relieved with supplemental oxygen, an inhaled broncho- minutes. The onset of action is immediate, and transient
dilator such as 2 or 3 puffs of metaproterenol (Alupent), and asystole (about 5 seconds) should be anticipated. An
subcutaneous administration of 0.1 mg (0.1 mL) of a 1:1000 alternative to adenosine is the calcium channel blocking
concentration of epinephrine, which may be repeated every agent diltiazem; a loading dose of 0.25 mg/kg is given
15 minutes. Isolated hypotension and tachycardia should by slow IV push. When these measures fail, a cardiolo-
respond to leg elevation, rapid infusion of IV fluids (nor- gist should be promptly called. In symptomatic patients,
mal saline or Ringers lactate), and 10 to 20 $g/kg/min of immediate synchronized cardioversion is warranted.
dopamine (as needed). Ventricular tachycardia (VT) has a regular wide com-
plex QRS (!0.12 sec) on an electrocardiogram. When
Severe Contrast Agent Reaction caused by guidewire manipulation in the heart, it is usu-
Life-threatening reactions to contrast (heralded by severe ally transient and reverts with a chest thump or having the
bronchospasm or laryngospasm, profound hypotension, patient cough vigorously. Symptomatic or hemodynami-
convulsions, or cardiac dysrhythmias) are exceedingly cally unstable patients with this dangerous rhythm re-
rare. These events require immediate, aggressive treat- quire immediate cardioversion with a synchronized shock
ment with supplemental oxygen, rapid IV fluid infusion, (200 watt-sec). Asymptomatic sustained (!30 sec) mono-
and IV administration of 0.1 mg (1 mL) of a 1:10,000 con- morphic VT is treated with amiodarone.77 The initial dose is
centration of epinephrine. The dose may be repeated every 150 to 300 mg given IV over 5 to 10 minutes followed by
2 to 3 minutes. Epinephrine must be given with care in an infusion of 1050 mg/day. The onset of action is almost
patients with cardiac dysrhythmias, coronary artery dis- immediate. Major side effects include confusion, seizures,
ease, or those undergoing treatment with nonselective and cardiopulmonary depression. Alternative agents in
beta-adrenergic blocking agents. These reactions may this situation include procainamide and ajmaline.
progress to complete cardiovascular collapse.
Sepsis
Hypoglycemia Bacteremia is a concern during nonvascular interven-
Patients with diabetes who receive insulin or oral hypo- tions, particularly those that involve manipulation of
glycemic agents may become hypoglycemic during the abscesses or the biliary and urinary systems.78 Fever,
procedure. Symptoms may include mental confusion, chills, or rigors are common; frank septic shock occurs
agitation, tremors, seizures, and cardiac arrest, which much less frequently. Broad spectrum antibiotics should
is rare. However, individuals with a profoundly low be started immediately if they have not already been
glucose level may be completely asymptomatic. If hypo- given. Rigors usually respond to 25 to 50 mg IV of
glycemia is suspected or detected, an infusion of 5% meperidine (Demerol). Hypotension from sepsis can
2. PATIENT EVALUATION AND CARE 43
be initially managed with IV saline boluses and a 10- to vein puncture sites is facilitated by elevating the patients
20-$g/kg/min infusion of dopamine. head. If a hematoma is present afterward, it should be
marked on the skin and documented in the patients chart.
Seizures
Seizures may be idiopathic or a reaction to drugs given
Patient Monitoring
during the procedure (e.g., contrast agents). Treatment
includes protection of the patients airway and body, Initial postprocedure monitoring follows the same
supplemental oxygen, and 5 to 10 mg IV of diazepam protocol as that used during the intervention. After arte-
(Valium) or 1 mg IV of midazolam (Versed) as needed. rial catheterization, the puncture site and distal pulses
should be checked throughout the observation period:
Air Embolism for example, every 15 minutes for 1 hour, every 30 minutes
This event is a rare occurrence during vascular access for the next hour, and every hour thereafter. The length
placement.79 Most patients remain asymptomatic, but of outpatient monitoring varies with the type of procedure
hypoxia and hypotension can occur. Some experts advo- and the method of hemostasis (manual compression
cate placing the patient in a left lateral decubitus position or closure device). Generally, patients are observed for 30
to prevent air from entering the right ventricular outflow to 90 minutes after the last dose of sedatives or analgesics
tract. Unfortunately, by the time the event is detected by is given and until institutional discharge criteria are
fluoroscopy, air has usually migrated into the pulmonary met. After diagnostic femoral or brachial arteriography, a
arteries. Air embolism is rarely fatal. Treatment usually is 4- to 6-hour observation period is routine (unless a closure
supportive, including supplemental oxygen, IV fluids, device is used). After diagnostic femoral or jugular venog-
and continuous patient monitoring. raphy, a 2- to 4-hour observation period is common.
Cardiopulmonary Arrest
Cardiorespiratory collapse may result from the patients Orders
underlying condition (e.g., massive pulmonary embolus, Patient orders should include the following directions:
multiorgan failure) or some aspect of the procedure itself
(e.g., contrast agent reaction, oversedation). Regardless of Vital signs and access site checks: Monitoring
the cause, basic life support maneuvers must be started usually is done every 15 minutes for the first hour
immediately, including alerting a code team, establishing and then tapered over the observation period.
an airway, and beginning cardiopulmonary resuscitation. Activity: The patient is kept at bed rest until near
the end of the monitoring period.
Pain control: Immediate postprocedure analgesia
POSTPROCEDURE CARE is primarily accomplished with oral and paren-
teral opioids.80
Diet: After sedatives and analgesics wear off,
Vascular Catheter Removal patients can be given liquids or a soft solid meal.
Catheters are withdrawn immediately after vascular Hydration: IV hydration usually is continued
and interventional procedures unless ongoing interven- throughout the postprocedure period if intravascu-
tion is necessary (e.g., overnight thrombolysis, abscess lar contrast was given. IV access should be main-
drainage). Additional lidocaine is given at the puncture tained while the patient recovers from moderate
site if sheath dwell time has been more than several sedation.
hours. Especially prior to arterial catheter removal,
blood pressure should be well controlled. The risk of
Management of Acute Complications
hemorrhagic complications can be reduced in patients
who have received heparin if catheter removal is de- Identification and management of delayed complica-
layed until the activated clotting time (ACT) falls into tions of various vascular and interventional procedures
the high-normal range (typically less than 200 seconds). are considered in detail in Chapter 3. The most common
Specific details of puncture site hemostasis and use of acute angiographic complications are described here.
compressive dressings or arterial closure devices are con- Puncture site bleeding or hematoma in most cases
sidered in Chapter 3. For arterial punctures, manual com- produces localized firm swelling. Treatment includes
pression is applied directly at, above, and below the punc- prolonged local compression and correction of any
ture site to stop bleeding but maintain blood flow. Pressure precipitating factors (e.g., coagulopathy, hypertension).
is applied for 10 to 20 minutes or until bleeding has If the patient has received heparin and hemostasis
stopped. Femoral vein punctures usually need about 5 to cannot be achieved in a reasonable period, protamine
10 minutes of compression. Hemostasis at internal jugular sulfate can be used to reverse anticoagulation.81 By itself,
44 I. BASIC PRINCIPLES AND TECHNIQUES
60. Klein LW, Miller DL, Balter S, et al. Occupational health hazards in 71. Waybill MM, Waybill PN. A practical approach to hypertension in
the interventional laboratory: time for a safer environment. J Vasc the 21st century. J Vasc Interv Radiol 2002;14:961.
Interv Radiol 2009;20:147. 72. Marik PE, Varon J. Perioperative hypertension: a review of current
61. Reddy P, Liebovitz D, Chrisman H, et al. Infection control practices and emerging therapeutic agents. J Clin Anesth 2009;21:220.
among interventional radiologists: results of an online survey. 73. Nayak KR, White AA, Cavendish JJ, et al. Anaphylactoid reactions
J Vasc Interv Radiol 2009;20:1070. to radiocontrast agents: prevention and treatment in the cardiac
62. Hansen ME, Miller III GL, Redman HC, et al. Needle-stick catheterization laboratory. J Invasive Cardiol 2009;21:548.
injuries and blood contacts during invasive radiologic proce- 74. Davidson CJ, Erdogan AK. Contrast media: procedural capacities
dures: frequency and risk factors. AJR Am J Roentgenol 1993; and potential risks. Rev Cardiovasc Med 2008;9:S24.
160:1119. 75. Patel A, Markowitz SM. Atrial tachycardia: mechanisms and man-
63. Baffoy-Fayard N, Maugat S, Sapoval M, et al. Potential exposure of agement. Expert Rev Cardiovasc Ther 2008;6:811.
hepatitis C virus through accidental blood contact in interven- 76. Holdgate A, Foo A. Adenosine versus intravenous calcium chan-
tional radiology. J Vasc Interv Radiol 2003;14:173. nel antagonists for the treatment of supraventricular tachycardia
64. Hansen ME, McIntire DD, Miller III GL. Occult glove perforations: in adults. Cochrane Database Syst Rev 2006;18:CD005154.
frequency during interventional radiologic procedures. AJR Am J 77. Trappe HJ. Treating critical supraventricular and ventricular
Roentgenol 1992;159:131. arrhythmias. J Emerg Trauma Shock 2010;3:143.
65. Solomon R, Werner C, Mann D, et al. Effects of saline, mannitol, 78. Smith TP, Ryan JM, Niklason LE. Sepsis in the interventional
and furosemide on acute decreases in renal function induced by radiology patient. J Vasc Interv Radiol 2004;15:317.
radiocontrast agents. N Engl J Med 1994;331:1416. 79. Vesely T. Air embolism during insertion of central venous
66. Patatas K, Koukkoulli A. The use of sedation in the radiology catheters. J Vasc Interv Radiol 2001;12:1291.
department. Clin Radiol 2009;64:655. 80. Hatsiopoulou O, Cohen RI, Lang EV. Postprocedure pain manage-
67. Martin ML, Lennox PH. Sedation and analgesia in the interven- ment of interventional radiology patients. J Vasc Interv Radiol
tional radiology department. J Vasc Interv Radiol 2003;14:1119. 2003;14:1373.
68. American Society of Anesthesiologists Task Force on Sedation 81. McEvoy GK, editor. AHFS Drug Information 2002. Bethesda
and Analgesia by Non-anesthesiologists. Practice guidelines for (MD): American Society of Health-System Pharmacists, 2002.
sedation and analgesia by non-anesthesiologists. Anesthesiology p. 1453.
2002;96:1004. 82. Levy JH, Adkinson Jr NF. Anaphylaxis during cardiac surgery:
69. Gozal D, Gozal Y. Pediatric sedation/anesthesia outside the implications for clinicians. Anesth Analg 2008;106:392.
operating room. Curr Opin Anesthesiol 2008;21:494. 83. Bashore TM, Gehrig T. Cholesterol emboli after invasive cardiac
70. McEvoy GK, editor. AHFS Drug Information 2002. Bethesda (MD): procedures. J Am Coll Cardiol 2003;42:217.
American Society of Health-System Pharmacists; 2002.
C H A P T E R
3
Standard Angiographic
and Interventional Techniques
Karim Valji
VASCULAR ACCESS artery [SFA] or deep femoral artery [DFA]), the risk of
thrombosis, pseudoaneurysm, or arteriovenous fistula
formation is significantly increased.6,7 If the puncture is
Anesthesia (Online Videos 3-1 and 3-2) too high (into the external iliac artery above the inguinal
A local anesthetic is given at the start of every angio- ligament), the risk of retroperitoneal or intraperitoneal
graphic or interventional procedure. The preferred agent bleeding is increased.8 The bony landmarks for the in-
is 1% or 2% lidocaine (Xylocaine), which inhibits sodium guinal ligamenta line running from the anterior supe-
channels involved in the conduction of nerve impulses. rior iliac spine to the pubic tubercleprovide only a
An intradermal skin wheal is made with a 25-gauge rough approximation.9
needle. The deeper subcutaneous tissues are anesthe- A small, superficial skin nick is made directly over the
tized with a long 22- or 25-gauge needle. Intravascular arterial pulse. A clamp is used to dissect the subcutane-
injection must be avoided by intermittent aspiration. The ous tissues. Although the advantages of real-time sono-
pain from lidocaine injection is caused by the low pH of graphic guidance for femoral artery puncture are obvi-
commercially available preparations. Discomfort is eased ous (Fig. 3-2), many practitioners continue to rely on the
with buffered lidocaine, which is prepared by admix- traditional method of manual palpation of the artery
ing the drug with sodium bicarbonate (1 mL of 0.9% unless entry is difficult. A pulsatile artery may be sur-
NaHCO3 solution in 10 mL of 1% lidocaine).1 Patients prisingly hard to puncture if the skin nick is malposi-
with a lidocaine allergy may receive an ester- rather than tioned, the artery is unusually mobile, underlying dis-
an amine-based anesthetic (e.g., 1% chloroprocaine).2 ease exists, or vasospasm follows repeated attempts. In
these situations, the operator should consider making a
second skin nick directly over the arterial pulse or at a
Retrograde Femoral Artery Catheterization
slightly higher location, waiting until a strong pulse has
(Online Video 3-2) returned, or using the opposite groin. It is sometimes
In 1953, Sven Ivar Seldinger first described the method possible to catheterize the abdominal aorta even in the
for percutaneous arterial catheterization involving a face of iliac artery occlusion if some flow can be detected
needle, guidewire, and catheter.3 The common femoral by ultrasound in the CFA and an angled catheter and
artery (CFA) is the safest and simplest arterial access hydrophilic guidewire are used to traverse the occlusion.
route because it is large, superficial, usually disease free, The course of the artery is palpated while an 18-gauge
and can be compressed against the femoral head to close needle is advanced at a 45-degree angle toward the
the puncture. However, this approach should be avoided femoral head (Fig. 3-3). It is safer to use a 21-gauge
when the patient has a CFA aneurysm, local infection, micropuncture needle set in coagulopathic patients
overlying bowel, or a fresh incision. Within several (Fig. 3-4). If double-wall technique is used, the stylet is
weeks after placement, synthetic grafts in the groin also removed after bone is reached, and additional lidocaine
may be accessed safely using a single-wall needle. is injected. The hub of the needle is depressed and then
When the skin is entered over the bottom of the femo- slowly withdrawn until pulsatile blood returns. Many
ral head and the needle is angled at 45 degrees, the interventionalists prefer a single-wall entry into the ves-
needle usually enters the CFA at its midpoint4 (Fig. 3-1). sel. However, because single-wall needles have a bev-
The inguinal crease is a poor landmark for skin punc- eled tip, the tip may be partially subintimal despite brisk
ture.5 If the puncture is low (into the superficial femoral pulsatile blood return. Slow return of dark blood usually
47
48 I. BASIC PRINCIPLES AND TECHNIQUES
A B
Arterial Closure Devices (Online Video 3-6)
For more than 50 years, manual compression has been the
standard approach for obtaining hemostasis of vascular Suture
Complications FIGURE 3-9 Massive hemorrhage after right femoral artery cath-
eterization seen on axial computed tomography scan.
Specific complications of interventional procedures are
considered in subsequent chapters. Complications after
venous catheterization include bleeding or hematoma,
thrombosis, and infection. Even when large sheaths are
used, major events are seen in less than 5% of cases.
Table 3-1 outlines the most common adverse out-
comes from femoral artery catheterization.36-39 Minor
bleeding or hematoma formation occurs in less than 10%
of simple femoral artery catheterization procedures.
Major bleeding requiring transfusion or surgical evacu-
ation is relatively rare (#1%), but more likely when
sheath size increases or anticoagulants and fibrinolytic
agents are used. Blood may collect in the thigh, groin,
retroperitoneum, or, rarely, the peritoneal space. Retro- A C
peritoneal hemorrhage should be suspected in a patient
with an unexplained drop in hematocrit, hypotension,
or flank pain (Fig. 3-9).
With proper technique, catheterization-related pseu-
doaneurysms are relatively uncommon (about 1% to
6%); arteriovenous fistulas are quite rare39,40 (see Fig. 1-34).
Most small (#2 cm) pseudoaneurysms close sponta-
neously. Large or persistent lesions require treatment
(Fig. 3-10, see later discussion). Femoral artery thrombosis
or occlusion usually is caused by dissection, spasm, or
pericatheter clot (Fig. 3-11). Cholesterol embolization larger sheaths and anticoagulants]).18,43 This vessel is
from traumatic disruption of an atherosclerotic plaque is more prone to thrombosis or pseudoaneurysm formation
a rare but potentially devastating complication of arteri- than the CFA (see Fig. 9-14). Distal neuropathy is a dis-
ography41 (see Chapter 2). tinct but uncommon sequela of brachial artery puncture
Other potential adverse events include nausea and related to the tight anatomic space shared by the artery
vomiting, vasovagal reactions, and contrast mediarelated and several peripheral nerves (see earlier discussion).
reaction or nephropathy. Cardiac events (e.g., arrhyth- Thus even small hematomas can cause nerve compres-
mias, angina, heart failure) and neurologic events (e.g., sion. Sensory or motor neuropathy is reported in about
seizures, femoral nerve injury, stroke) also can occur dur- 2% to 7% of patients who undergo this procedure.16-18,43
ing vascular interventions.42 The deficit is more likely to become permanent if early
The reported frequency of complications from axillary surgical decompression is not accomplished as soon as
or brachial artery access ranges from 2% to 24%.16-18,20 In the problem is suspected. The other devastating neuro-
contemporary series, catheterization-related events with logic complication of retrograde brachial artery catheter-
mid or low brachial artery puncture are less common but ization is cerebral embolization of pericatheter clot,
not negligible (0.44% [for diagnostic studies with 4-Fr which has been reported in up to 4% of cases but is much
catheters] to 6.5% [for interventional procedures with less common in actual practice.17
A B
C
54 I. BASIC PRINCIPLES AND TECHNIQUES
Treatment of Postcatheterization pseudoaneurysm away from the neck (see Fig. 3-10).
Bovine thrombin (1000 units/mL) is injected into the
Pseudoaneurysms and Arteriovenous
lesion over 5 to 10 seconds. Most pseudoaneurysms
Fistulas require well under 1000 units for complete thrombosis.
Ultrasound-guided compression repair is effective in many Clot formation is monitored with color Doppler imag-
cases of postcatheterization pseudoaneurysms.44-46 In ing. The success rate is 90% or greater, even in the face
this technique, the ultrasound transducer is used to of anticoagulation. Complete closure may be more prob-
compress the neck of the pseudoaneurysm while flow is lematic with complex pseudoaneurysms.48 A failed first
maintained in the SFA (Fig. 3-12). Patients are then kept attempt should be repeated. However, the patient and
at bedrest for 4 to 6 hours. Follow-up sonography is operator should be aware that prior exposure to throm-
required to confirm permanent thrombosis. Pseudoan- bin (topical or otherwise) can lead to antibody formation
eurysm closure is successful in about 75% to 85% of and the small risk of anaphylactic reaction. Although
cases. However, the method is painful (usually requiring complications are rare, there are several reports of limb-
moderate sedation), time-consuming, and sometimes threatening embolization or downstream thrombosis.53-55
ineffective, particularly in patients receiving anticoagu- The presence of a wide or short aneurysm neck may
lation.47 Compression repair is not advised when flow in predispose to this serious event.
the neck cannot be obliterated or for lesions located Arteriovenous fistulas are much less common than
above the inguinal ligament. pseudoaneurysms after femoral artery catheterization
Ultrasound-guided percutaneous thrombin injection has (Fig. 3-13 and see Fig. 1-34). Many fistulas close spontane-
become the first-line treatment for angiography-related ously. Repair is recommended if they persist for more
pseudoaneurysms.46-51 Thrombin injection also has been than 2 months, increase twofold or more in size, or
used to treat postcatheterization brachial artery pseu- become symptomatic. As an alternative to operation, cov-
doaneurysms.52 The procedure is quick, relatively pain- ered stents have been deployed to close fistulas. However,
less, and highly effective. After excluding an arteriove- the published experience is too limited to endorse this
nous fistula and using real-time ultrasound guidance, a approach as a routine measure.56-58 In rare instances, em-
22- or 25-gauge needle is inserted into the body of the bolization of a long track is feasible (see Fig. 8-53).
A B
FIGURE 3-12 Ultrasound-guided compression repair of a postcatheterization pseudoaneurysm. A, Color Doppler sonogram shows a large
pseudoaneurysm (p) arising from the left common femoral artery with classic to-and-fro flow at the aneurysm neck. B, After 30 minutes of
compression of the neck, the pseudoaneurysm has thrombosed. Flow is maintained in the femoral artery (A) and vein (V).
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 55
B
FIGURE 3-16 Methods for reforming a Simmons catheter. (Adapted from Kadir S. Diagnostic angiography. Philadelphia: WB Saunders; 1986. p. 74.)
In the equation, !P $ pressure gradient, Q $ blood flow, to use a single catheter to measure a pullback pressure
L $ length of the stenosis, " $ blood viscosity, and r $ across the lesion. With this method, however, the gradient
radius. In medium-sized arteries, blood flow is un- may be spuriously elevated if the diameters of the catheter
changed until the luminal diameter is reduced by 50%, and vessel are similar (e.g., arteries %5 mm in diameter).
which corresponds to a cross-sectional area reduction of A useful tool for determining hemodynamic significance
75% (Fig. 3-19). Blood flow falls precipitously as the of lesions in medium- and small-caliber arteries is a pres-
diameter stenosis approaches 75% (about a 95% reduc- sure guidewire (e.g., PrimeWire Prestige).65,66
tion in cross-sectional area). The relationship between
flow reduction and luminal diameter becomes more
Contrast Agents
complex with diffuse disease or tandem lesions. Pres-
sure gradients are affected by blood flow. For example, Standard contrast materials used for vascular and inter-
as the peripheral arterial resistance in the legs drops ventional procedures are iodinated organic compounds.
with exercise, the magnitude (and therefore the clinical
Ionic monomeric agents have a single triply iodin-
significance) of proximal pressure gradients increases.
ated benzene ring and form salts in plasma.
The thresholds used to define a significant arterial
Ionic dimeric agents (e.g., ioxaglate) contain twice
pressure gradient are controversial. Resting systolic and
the number of iodine atoms per molecule.
mean gradients from 5 to 34 mm Hg have been sug-
Nonionic monomeric agents are less toxic because
gested.62-64 Absolute or relative gradients after flow aug-
of lower osmolality, nondissociation in solution,
mentation (intraarterial injection of a vasodilator) are
and increased hydrophilicity.
favored by some experts. As a general rule, a resting
Nonionic dimeric agents are isosmolar (or nearly
systolic gradient of 10 mm Hg or greater is considered
so) with plasma and are the least toxic of the
significant in the arterial system. In the central veins,
available materials.
a focal gradient of 3 to 6 mm Hg or greater can be flow-
limiting. Iodinated contrast agents can produce numerous sys-
Pressure gradients are most accurate when simultane- temic effects after intravascular administration67 (Box 3-2).
ous measurements are obtained from endhole catheters on The severity of these alterations depends largely on the
either side of a stenosis. However, often it is more practical osmolality of the preparation. At similar iodine concen-
trations, low osmolar contrast materials (LOCMs; ionic
dimers and nonionic agents) have a significantly lower
Percent stenosis (1-A/Ao)100 osmolality (600 to 800 mOsm/kg) than high osmolar con-
0 20 40 60 80 90 95 99 100 trast material (HOCMs; ionic monomers) with osmolality
100 at 1400 to 2000 mOsm/kg. Iodixanol (Visipaque) is the only
80
BOX 3-2
Percent maximum pressure drop
Peripheral resistance
Percent maximum flow
isosmolar agent (290 mOsm/kg) currently available in the Carbon dioxide has been used extensively as a contrast
United States. agent for digital imaging in a variety of arterial and
In most centers, nonionic agents are chosen for all venous beds76-80 (Fig. 3-20). The gas rapidly dissolves in
intravascular applications. Minor side effects, such as blood and is eliminated from the lung less than 30 seconds
nausea, vomiting, and local pain, are much less common after injection. There is no risk of allergic reaction or neph-
with these drugs.67 The overall incidence of adverse rotoxicity. An airtight system of reservoir bag, tubing,
events with LOCM is less than 1%. The frequency of and syringes is constructed to purge a delivery syringe of
moderate to severe reactions is estimated at about 0.1% room air and substitute instrument grade CO2 (Online
to 0.2% for HOCM and 0.01% to 0.02% for LOCM. The Video 3-10). For abdominal aortography or inferior vena-
frequency of fatal reactions is less than 0.005% and cavography, a 60-mL syringe is required. The catheter
not significantly different between the two classes of is then primed with the gas before rapid injection. Some
material.68 There are only small differences in imaging patients experience discomfort with injection. The quality
quality among the various agents at the same iodine of images is generally inferior to those obtained with
concentration,69,70 The evidence is strong but not indis- iodinated contrast. In addition, complications can arise
putable that contrast nephropathy is less likely in at-risk from gas trapping and vapor lock, especially in the
patients with use of iodixanol.71-75 At centers in which pulmonary artery, abdominal aortic aneurysms, and the
cost issues are of particular concern, an argument can be inferior mesenteric artery. The agent cannot be used in arter-
made for selective use of nonionic material. ies above the diaphragm because of the risk of intracerebral
In patients with renal dysfunction or a history of life- embolization.
threatening allergy, alternative contrast agents should be Gadolinium-based contrast materials can be used in indi-
considered. Use of these media may limit or completely viduals with a history of anaphylactic reaction to iodin-
eliminate the need for iodinated material. ated agents and normal renal function. However, they
A B
C
60 I. BASIC PRINCIPLES AND TECHNIQUES
are not safe for intravascular use in patients with acute There is also growing support for its additive benefit in
renal failure, chronic kidney disease (eGFR [estimated preventing restenosis after some endovascular recanali-
glomerular filtration rate] #30 mL/min), or dialysis zation procedures.93 Significant drug interactions can
dependence. In these populations, there is clear dose- occur with certain cytochrome P450 inhibitors (e.g., dil-
related causation between some of these drugs and the tiazem, erythromycin, and omeprazole).
highly debilitating disorder of nephrogenic systemic #IIB$3 Integrin (GP IIb/IIIa) receptor inhibitors are a
fibrosis81-83 (NSF, see Chapter 2). class of potent cell receptor antagonists that act on the
final common pathway to platelet aggregation. Al-
Pharmacologic Adjuncts though interplatelet binding is inhibited, platelet
attachment to subendothelial elements is maintained.
Antiplatelet Agents Although these parenteral drugs have great potential
Aspirin (acetylsalicylic acid, ASA) is a moderate inhibitor for enhancing revascularization in acute coronary syn-
of platelet aggregation. It works by irreversibly inacti- dromes, the experience in peripheral arterial disease
vating cyclooxygenase (COX), a critical enzyme in the has been somewhat disappointing.94-96 As such, these
production of a key enzyme (thromboxane A2) required agents should not be used routinely but instead should
for platelet function.84,85 The drug is rapidly absorbed be reserved for selected cases, such as slow response to
from the stomach; platelet function is inhibited within thrombolytic agents, thrombophilic states, need for
1 hour of ingestion and continues for the lifetimes of rapid revascularization, or infrageniculate interven-
existing platelets (about 7 to 10 days). Aspirin prolongs tions (Table 3-3). It is important to carefully monitor
the bleeding time without significantly affecting other platelet levels, which can fall precipitously during
coagulation parameters. Patients often are maintained treatment.
on a daily dose of 325 mg for at least several months
after recanalization procedures. Antithrombin Agents
Thienopyridines are more potent oral antiplatelet Heparin is a polyanionic protein that binds with anti-
agents that irreversibly inhibit binding of adenosine di- thrombin (AT), among other plasma proteins and cells.97
phosphate (ADP) to platelet receptors, thus preventing The resulting complex inhibits clot formation by inacti-
platelet-fibrinogen binding and &IIB'3 integrin (glyco- vating thrombin and factor Xa. This effect is dependent
protein [GP] IIb/IIIa)mediated platelet activation and on a specific pentasaccharide sequence present on un-
aggregation.86,87 The first-generation agent ticlopidine fractionated heparin and other synthetic drugs (see later
(Ticlid) is rarely prescribed because of certain relative discussion). Because thrombin is the critical enzyme in
drawbacks. The second-generation drug clopidogrel (Plavix) clot formation, heparin is a potent antithrombotic agent.
is in widespread use. The standard loading dose is The drug is cleared from the body in two phases. Rapid
300 mg orally, with typical daily dosage of 75 mg. The initial clearance by fairly indiscriminate binding to
new third-generation agent prasugrel may be useful in plasma proteins and endothelial cells is followed by
patients who are nonresponders to clopidogrel.86 slower clearance by the kidneys. The biologic half-life
Combination therapy (aspirin ( clopidogrel) is favored varies widely among individuals, but it is roughly
in many situations for patients with coronary artery dis- 1 hour at typical therapeutic doses (5000 units IV bolus
ease. However, current recommendations favor mono- followed by 500 to 1500 units/hr infusion). Protamine, a
therapy for primary prevention of cardiovascular events
in the subset of individuals with peripheral arterial
disease.88,89 For interventionalists, clopidogrel (alone or
in combination with aspirin) may be useful in some pa- TABLE 3-3 &IIB'3 Integrin (GP IIB/IIIA) Platelet Inhibitor
tients following arterial recanalization procedures. These Agents
agents also show promise in preventing restenosis after
angioplasty, stent insertion, or bypass graft placement. Generic
(Trade Name) Structure Half-Life Dosage
The major downside to thienopyridines is bleeding. In
patients requiring certain invasive procedures, clopido- Abciximab Monoclonal 8-12 hr Bolus 0.25 mg/kg
grel must be withheld for 7 to 10 days to reverse the (ReoPro) antibody Infuse 0.125 )g/kg/min
over 12 hr
bleeding tendency.
Eptifibatide Synthetic 2.5 hr Bolus 180 )g/kg
Cilostazol (Pletal) is a phosphodiesterase III inhibitor (Integrilin) peptide t $ 0,10 min
that has antiplatelet, antithrombotic, smooth muscle an- Infuse 2.0 )g/kg/min
tiproliferative, and vasodilatory effects.90-92 There is over 18-24 hr
abundant evidence that long-term therapy (50 to 100 mg Tirofiban Nonpeptide 2 hr Bolus 0.10 )g/kg
(Aggrastat) tyrosine Infuse 0.15 )g/min
orally twice daily) increases exercise ability and overall
over 18-24 hr
quality of life in patients with intermittent claudication.
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 61
cationic protein derived from salmon sperm, completely agents that inhibit both free and circulating thrombin. Un-
reverses the anticoagulant effect (see Chapter 2). like heparin-related compounds, they do not require anti-
Because heparin pharmacokinetics are unpredictable, thrombin for activity.103,105,106 The anticoagulative effect is
its effect must be measured. During vascular proce- much more predictable than with unfractionated heparin.
dures, the antithrombotic response can be followed with Whereas they are used widely during coronary interven-
the activated clotting time (ACT), which reflects whole tions, experience in other vascular beds is limited.107,108
blood clotting.98 Normal and therapeutic ranges are spe- However, these drugs play a crucial role in patients with a
cific to each manufacturers device. The activated partial history of HIT.109
thromboplastin time (PTT) is used to monitor long-term Warfarin (Coumadin) is an oral antithrombotic agent
anticoagulation. The therapeutic range is 1.5 to 3.5 times that inhibits vitamin Kdependent liver synthesis of the
the control value.99 One protocol for adjusting heparin proenzymes for coagulation factors II, VII, IX, and X.110
doses based on the PTT obtained every 4 to 6 hours was Despite many drawbacks (including inconsistent dose-
recently proposed by a panel of experts.100 Patients who response, need for frequent monitoring, and nontrivial
are extremely resistant to heparin may require titration bleeding complications), warfarin is still widely used to
by direct heparin assay or a switch to a low molecular prevent and treat arterial and venous thrombotic events.
weight heparin (LMWH) agent (see later discussion). It has a half-life of 36 to 42 hours. A full anticoagulative
The major complications of heparin therapy are effect is not achieved until 3 to 7 days after therapy is
bleeding, heparin-induced thrombocytopenia (HIT) (see started. Drug monitoring and reversal are discussed in
Chapter 1), and osteopenia (with long-term use). The Chapter 2. A wide variety of foods and medications can
risk of bleeding is a function of drug dose, concomitant potentiate or inhibit the anticoagulant effect of warfarin.
use of thrombolytic agents, recent surgery or trauma,
baseline coagulation status, kidney function, and age. To Antispasmodic Agents
screen for HIT, platelet levels should be monitored two Vasodilators are used during vascular procedures to pre-
or three times a week. vent or relieve vasospasm and occasionally to augment
LMWH has more predictable and persistent antico- arterial flow.111 One of the more commonly used agents is
agulant activity than unfractionated heparin.97,101,102 This the direct smooth muscle relaxant nitroglycerin (100 to
class of drugs includes enoxaparin (Lovenox), dalteparin 200 )g IA or IV), which has a half-life of 1 to 4 minutes.
(Fragmin), reviparin, and tinzaparin (Innohep). The pri- Calcium channel blockers, including verapamil, can be
mary mechanism of action is inhibition of factor Xa and used also. This drug class is contraindicated in patients
thrombin mediated through antithrombin. Unlike un- with elevated intracranial pressure and certain cardiac
fractionated heparin, LMWH exhibits almost no indis- conditions. Adverse effects include hypotension, tachy-
criminate cellular or protein binding. As such, clearance cardia, and nausea. However, these reactions are uncom-
is dose-independent, and the half-life (about 4 hours) is mon with standard dosages.
much longer. The dose must be reduced in patients with
renal disease; the drug is avoided altogether in severe
renal insufficiency (eGFR #30 mL/min). VASCULAR INTERVENTIONAL
LMWH is becoming the standard prophylactic regi- TECHNIQUES
men in prevention of deep venous thrombosis (e.g., be-
fore major orthopedic or abdominal surgery) and often
Balloon Angioplasty
replaces the heparin/warfarin sequence for treatment of
acute deep venous thrombosis.102,103 Major advantages Percutaneous transluminal balloon angioplasty (PTA)
over unfractionated heparin include ease of administra- remains the first line minimally invasive technique for
tion (once or twice daily by subcutaneous injection), no treatment of stenoses in the vascular, biliary, and urinary
need for monitoring, and a low (#2%) frequency of HIT.97 systems (Fig. 3-21). PTA was conceived by Dotter and
Bleeding is still a major concern with long-term use. Judkins,112 who first used sequential dilators to open an
Fondaparinux (Arixtra) is a synthetic pentasaccharide occluded SFA. Gruentzig113 is credited with the develop-
that corresponds to the critical portions of the heparin ment of balloon angioplasty catheters that are the basis
molecule responsible for binding to antithrombin.97 It of the current method. In many situations, PTA is per-
only targets factor Xa and has a much longer half-life formed in conjunction with stent placement to obtain
(about 17 hours) than heparin-related agents. One draw- optimal results (see later discussion).
back of this drug is the lack of an available reversing
agent. On the other hand, it may be prescribed in pa- Mechanism of Action
tients with a history of HIT.104 Inflation of an angioplasty balloon in a stenotic artery
Direct thrombin inhibitors (bivalirudin [Angiomax], argatro- causes desquamation of endothelial cells, splitting or dis-
ban, and lepirudin [Refludan]) are recombinant or synthetic section of the atherosclerotic plaque and adjacent intima,
62 I. BASIC PRINCIPLES AND TECHNIQUES
A B
C D
FIGURE 3-23 Transplant hepatic artery rupture from excess pressure applied to an oversized angioplasty balloon. A, Critical stenosis of
liver transplant arterial stenosis (arrow) on celiac arteriogram. B, First balloon treatment failed to break the stenosis. A second balloon that was
2 mm larger than the calculated vessel diameter was inflated above the recommended pressure. The balloon ruptured. C, Arteriography shows
contained rupture beyond the anastomosis (arrow). D, After successful passage of a guidewire, treatment with intravenous heparin and intraar-
terial nitroglycerin, stent placement reestablished flow in the artery.
A B
FIGURE 3-24 Balloon angioplasty of eccentric right superficial femoral artery stenosis (A) produces a widely patent vessel (B).
A B
FIGURE 3-25 Hepatic artery dissection from guidewire manipulation. A, Celiac arteriogram after embolization of the gastroduodenal
artery (curved arrow) and retroduodenal artery (arrowhead) in preparation for radiotherapy for hepatocellular carcinoma. Coils were placed in
the presumed right gastric artery. The coils migrated to the proper hepatic artery (PHA). B, Attempts to snare and remove them caused
formation of an occlusive dissection of the PHA that extended into the right and left hepatic arteries (arrows).
prevent the rigid catheter tip from injuring the vessel as If pain persists after deflation, vessel rupture must be ex-
the balloon expands. The waist produced by an ath- cluded with angiography while maintaining guidewire
erosclerotic stenosis yields suddenly as the plaque access. If the vessel has ruptured, the balloon is immedi-
cracks. Venous stenoses sometimes open more gradu- ately reinflated across the site for 5 to 10 minutes to pre-
ally. Optimal inflation parameters (number, duration, vent bleeding. By itself, this maneuver may seal the tear.
and pressure) are not firmly established outside the If not, a stent (uncovered or covered depending on the
coronary circulation. Venous stenoses sometimes require vessel) can be inserted122 (see Fig. 19-13). Urgent operative
two to three inflations of 30 to 120 seconds to achieve a repair is hardly ever necessary.
good result. It is standard teaching that a guidewire remain across
Patients may express mild discomfort during balloon the lesion while the deflated balloon is withdrawn and
inflation. If the patient complains of severe pain, the bal- postangioplasty angiography is done. However, many
loon should be immediately deflated unless the operator interventionalists abandon stenoses in large arteries
is confident that the balloon is not significantly oversized. and veins. If a sheath or guiding catheter is being used,
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 65
I N D I C AT I O N S F O R S T E N T A D VA N T A G E S O F S T E N T
PLACEMENT DESIGNS
AVF, arteriovenous fistula; CFA, common femoral artery; TIPS, transjugular intrahepatic
portosystemic shunt.
Stents may have U.S. Food and Drug Administration nitinol (a nickel/titanium alloy) or the metallic alloy
approval or European CE mark for use in particular Elgiloy. The final diameter of the stent is a function of
vascular beds. If a physician chooses to use a device the outward elastic load of the stent and the inward
off-label, the patient should consent to this deci- forces of elastic wall recoil or extrinsic compression.
sion. Stent selection is based on a variety of factors For vascular use, nominal diameters are 4 to 24 mm for
(Box 3-6); a very simplified algorithm is outlined in placement through 5- to 12-Fr sheaths. Stents are over-
Table 3-4. sized by 1 to 2 mm (and even more in large veins)
Self-expanding stents are compressed onto a catheter to ensure firm vessel apposition and prevent migra-
and deployed by uncovering a constraining sheath or tion. When the path to the lesion is tortuous or steeply
membrane (Figs. 3-26 and 3-27). Most are composed of angled (e.g., over the aortic bifurcation), these stents
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 67
A B
A B C
D E
FIGURE 3-30 Combined pulse-spray and infusion thrombolysis of an occluded femoropopliteal bypass graft. A, The graft is occluded at
its origin (arrow). B, After pulse-spray thrombolysis with bolus dose of fibrolytic agent, significant clot lysis has occurred. C, After overnight
infusion of the drug, the body of the graft is almost entirely free of clot. D, A long stenosis in the distal popliteal artery and tibioperoneal trunk
is revealed. E, After balloon angioplasty, the graft outflow is significantly improved.
TABLE 3-5 Fibrinolytic Agent Dosing Regimens surgically, depending on the nature of the occlusion and
the condition of the patient.
Maximum Maximum
Complications directly related to revascularization
Agent Infusion Dose Bolus Dose
of the extremities include reperfusion syndrome and com-
t-PA 0.5-1.0 mg/hr 10 mg 40 mg partment syndrome. Revascularization of a nonsalvage-
0.001-0.02 mg/kg/hr
able necrotic limb can release lactic acid, myoglobin,
Reteplase 0.25-1.0 U/hr 2-5 U 20 U
and other substances that may lead to acute kidney
72 I. BASIC PRINCIPLES AND TECHNIQUES
injury and cardiovascular instability. Bleeding into a 12% of cases. Finally, device failure is an occasional
treated (or even untreated) limb may significantly ele- problem with some catheters. However, these catheters
vate muscular compartment pressures and require play a critical role in patients at undue risk for bleeding
fasciotomy (Table 3-6). from fibrinolytic agents who are otherwise appropriate
candidates for endovascular thrombectomy.
There are a variety of devices available around the
Mechanical Thrombectomy world. Three of the more popular catheters are consid-
Percutaneous thrombectomy devices are emerging as an ered as follows:
attractive alternative or adjunct to enzymatic thrombol-
The Arrow-Trerotola percutaneous thrombectomy device
ysis or aspiration thrombectomy.162-165 Existing throm-
(PTD) is composed of a nitinol basket that acts
bectomy catheters can be classified by their mechanism
like an egg-beater on relatively fresh thrombus
of action as (1) clot maceration and aspiration or (2) clot
(Fig. 3-31). The device is placed over a guidewire
pulverization into microparticles. However, none of the
into the thrombus. The activated device spins at
available models has entirely lived up to expectations to
3000 rpm. The macerated clot is then aspirated
replace enzymatic thrombolysis by improving technical
through the sideport of a sheath. The PTD is
efficacy of clot removal and lowering the risk for ad-
primarily used in treatment of thrombosed
verse events. Adjunctive enzymatic lysis often is needed
hemodialysis access and iliofemoral deep vein
to complete thrombus removal. Bleeding complications
thrombosis.166-168 It may also have applications in
are not completely eliminated (up to 10% to 15% in some
other vascular territories (e.g., mesenteric veins,
series). The rate of distal embolization ranges from 5% to
pulmonary artery).
15%. Vessel perforation or dissection is reported in 5% to
The AngioJet thrombectomy catheter is a flexible
device that is inserted directly into the thrombus
(Fig. 3-32). Based on the Bernouilli principle,
TABLE 3-6 Complications of Enzymatic Thrombolysis high-speed saline jets exit the end of the
Complication Frequency (%) catheter, producing a low pressure space that
sucks clot into the catheter for maceration.
Minor puncture site bleeding 5-25
The clot fragments are propelled back through
Major bleeding requiring transfusion or surgery 3-7
Distal embolization 2-15 the catheter and evacuated from the body.
Pericatheter thrombosis The principal indications for use are iliofemoral
Reperfusion syndrome deep vein thrombosis and dialysis access throm-
Compartment syndrome bosis.169 However, it is widely used in other
Drug reactions
vascular beds.170 It has two main drawbacks:
Vessel or graft extravasation
the occasional occurrence of bradyarrythmias
FIGURE 3-31 Arrow-Trerotola mechanical thrombectomy device. (Images courtesy of Teleflex Medical/Arrow International.)
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 73
A B
C D
74 I. BASIC PRINCIPLES AND TECHNIQUES
For the treatment of hemorrhage, the goal of embolo- Materials and Technique
therapy is to reduce flow to the bleeding site and allow A vascular sheath is placed to maintain access in case the
endogenous clotting but still maintain collateral perfusion delivery catheter becomes occluded with embolic material.
to neighboring tissue (Fig. 3-34). For tissue obliteration or Delivery catheters must not have side holes through which
vascular malformation occlusion, the goal is to completely embolic material can escape. In some cases, the diagnostic
eliminate perfusion to or outflow from the target site catheter can be advanced without difficulty. Otherwise, a
(including potential collaterals) while preserving nearby coaxial microcatheter is inserted and directed to the target
tissue (see Fig. 10-34). Embolization has several advan- site using a steerable guidewire. Coils may get stuck in the
tages over surgery.176,177 Vital structures are not damaged lumen of some high-flow microcatheters, so an appropriate
en route to the bleeding site or organ, tissue loss is mini- device must be chosen. The outer catheter should be se-
mized by limiting occlusion to target vessels, and the risks cured in a stable position. In some cases (e.g., pulmonary
associated with an operation are avoided. With currently AVM occlusion), a larger guiding catheter or sheath is
available materials, superselective embolization is possi- advanced close to the proposed site of device placement.
ble almost anywhere in the body. In vascular systems with extensive collateral circu-
The decision to perform embolotherapy is based on lation (e.g., mesenteric and peripheral arteries), the
several factors, including the risks of embolization, the operator must be cognizant of potential routes of blood
feasibility and efficacy of alternative procedures, and the flow. In this situation, it may be imperative to close
experience of the operator. Beforehand, a thorough an- the back door to prevent rebleeding (see Figs. 8-54
giographic evaluation is needed to define the bleeding and 11-32).
site or abnormality, the path to the target, and the state A wide assortment of embolic agents are available for
of existing and potential collateral vessels. vascular occlusion (Table 3-7).
C
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 75
PERMANENT
Macrocoils P
Microcoils P
Amplatzer plug P
Polyvinyl alcohol (PVA) particles D
Microspheres D
Alcohol P, D
Sodium tetradecyl sulfate (SDS, 3%) P, D
Glue P, D
Onyx P, D
TEMPORARY
FIGURE 3-35 Macrocoil with loader.
Gelfoam pieces P
Occlusion balloon catheter P
Thrombin P
D, distal; P, proximal.
A
1 2 3 4 5 6
B
FIGURE 3-38 Amplatzer II vascular plug. A, Plug connected
to delivery catheter. B, Expanded plug in place in vessel. ( AGA
Medical. Reprinted with permission.) FIGURE 3-39 Gelfoam sheet and cut torpedoes.
3. STANDARD ANGIOGRAPHIC AND INTERVENTIONAL TECHNIQUES 77
52. Sheiman RG, Brophy DP, Perry LJ, et al. Thrombin injection for the nephropathy after angioplasty in chronic renal failure patients:
repair of brachial artery pseudoaneurysms. AJR Am J Roentgenol the ICON (Ionic versus non-ionic Contrast to Obviate worsening
1999;173:1029. Nephropathy after angioplasty in chronic renal failure patients)
53. Sadiq S, Ibrahim W. Thromboembolism complicating thrombin study. JACC Cardiovasc Interv 2009;2:415.
injection of femoral artery pseudoaneurysm: management with 74. Nie B, Cheng WJ, Li YF, et al. A prospective, double-blind, ran-
intraarterial thrombolysis. J Vasc Interv Radiol 2001;12:633. domized, controlled trial on the efficacy and cardiorenal safety of
54. DAyala M, Smith R, Zanieski G, et al. Acute arterial occlusion after iodixanol vs. iopromide in patients with chronic kidney disease
ultrasound-guided thrombin injection of a common femoral artery undergoing coronary angiography with or without percutaneous
pseudoaneurysm with a wide, short neck. Ann Vasc Surg 2008;22:473. coronary intervention. Catheter Cardiovasc Interv 2008;72:958.
55. Ohlow MA, Secknus MA, von Korn H, et al. Percutaneous thrombin 75. Jo SH, Youn TJ, Koo BH, et al. Renal toxicity evaluation and com-
injection for treatment of iatrogenic femoral artery pseudoaneu- parison between Visipaque (iodixanol) and Hexabrix (ioxaglate) in
rysms: a case for caution. Angiology 2008;59:372. patients with renal insufficiency undergoing coronary angiography:
56. Tsetis D. Endovascular treatment of complications of femoral the RECOVER study: a randomized controlled trial. J Am Coll Car-
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C H A P T E R
4
Percutaneous Biopsy
Hamed Aryafar, Thomas B. Kinney
Percutaneous biopsy is a widely used interventional tech- include hematocrit, platelet count, prothrombin time,
nique for obtaining tissue samples.1,2 The crucial element partial thromboplastin time, and international normal-
of the procedure is image guidance, which facilitates ac- ized ratio5 (INR) (see Chapter 2). Coagulopathies should
curate and safe needle passage. Percutaneous biopsy with be corrected with appropriate transfusions of platelets,
image guidance is less invasive and less expensive than fresh-frozen plasma, vitamin K, or packed red blood
most surgical methods. The procedure has become safer cells. Although institutional thresholds vary, transfu-
and more effective with advances in imaging, specialized sions should be considered when the INR is greater
cytologic analyses, and small-gauge, thin-walled needles. than 1.5 or when platelet count is less than 50,000/mm3.
Cross-sectional imaging with computed tomography However, numerous studies have shown the relatively
(CT), ultrasound, and magnetic resonance imaging (MRI) low predictive value of abnormal screening parameters
permits safe diagnosis of small, remote lesions that once in predicting bleeding.5,6 Surgical series also have indi-
were completely inaccessible in this way. The accuracy cated that preoperative coagulation studies correlate
of percutaneous biopsy for the diagnosis of malignancy poorly with postoperative bleeding.6 Recent Society
in the chest and abdomen is about 85% to 95%.3 Definitive of Interventional Radiology practice guidelines offer
diagnosis of benign lesions is less accurate, however. Fur- useful coagulation and transfusion parameters for
ther advances in biopsy and cytopathologic methods percutaneous biopsy depending on whether the lesions
should improve these results. are superficial (minimal risk); deeper intraabdominal,
The most common indication for percutaneous biopsy thoracic, or retroperitoneal (moderate risk); or renal
is the diagnosis of malignancy, including primary neo- (significant risk).7 Interventionalists must be careful to
plasms, metastatic disease, tumor staging, and recurrent screen their patients for use of potent antiplatelet agents
disease after treatment. The procedure also is used for such as clopidogrel (Plavix). These agents should be
diagnosis of inflammatory or infectious processes, abnor- discontinued at least 5 days before moderate or signifi-
mal fluid collections, and diffuse organ disease. Relative cant risk biopsies. Care should be taken before discon-
contraindications include uncorrectable coagulation ab- tinuing Plavix if it is prescribed to maintain patency
normalities, lack of a safe percutaneous pathway to the of a coronary artery stent. A cardiology consult may
lesion, and an uncooperative patient in whom motion be necessary to avoid stent complications based on type
may increase the risk of bleeding.4 Biopsy usually is not of stent used (drug-eluting vs. bare metal) and timing of
indicated in a patient who will undergo surgery regard- stent placement.8,9
less of the biopsy results or if the results will not change
the management of the patient (e.g., the patient is already
Materials
in hospice care).
A wide array of needles are available for percutaneous
biopsy procedures.10 Needles can be classified by caliber
TECHNIQUE or gauge, tip configuration, and mechanism of sample
acquisition. Needle sizes are divided broadly into
smaller gauge (20 to 25 gauge) and larger gauge (14 to
Patient Preparation 19 gauge).3 Thinner-gauge needles often provide ade-
The patients history, clinical status, and imaging stud- quate cytologic material and often histologic material as
ies should be reviewed and discussed with the refer- well. Smaller-caliber needles also minimize bleeding,
ring physicians. Routinely performed coagulation studies providing a margin of safety when multiple passes are
84
4. PERCUTANEOUS BIOPSY 85
required. Traversing bowel may at times be necessary, The vulnerability of organs along the anticipated
and complications can be minimized by using thin- path of the biopsy needle (e.g., pleura, bowel) may
gauge needles.4 However, they can be somewhat diffi- dictate needle selection, because smaller-gauge needles
cult to direct into lesions because they tend to deflect (!19 gauge) are relatively safe.
significantly, particularly in deep-seated lesions. Larger Preprocedure imaging characteristics also may guide
needles are easier to direct and provide better samples needle selection. For example, smaller-gauge needles are
for cytology and histology, often with fewer needle used for metastatic disease and in patients with a known
passes. The risk for hemorrhage may increase as primary malignancy. In patients with no known primary
needle size increases.5 Needles also are classified by malignancy at the time of biopsy or in patients with
tip configuration10 (Fig. 4-1). Needles vary in the angle suspected lymphoma, multiple passes with fine-gauge
and bevel of the tip. The Chiba and spinal needles needles or several passes with a large-gauge needle
have bevel angles of 25 and 30 degrees, respectively. often are required to obtain adequate tissue for diagno-
Greene, Madayag, and Franseen (or Crown) needles sis. Physician experience is an important factor; auto-
have 90-degree tips. Needle tips are classified also mated devices yield better results when the operator is
into noncutting (aspiration needles such as the Chiba less experienced at obtaining core material by manual
or spinal) and cutting (end-cut or side-cut) types. aspiration.
Needles can be manual, spring-loaded, or automated.
The wide selection of needle types suggests that no
Imaging Guidance
design is clearly optimal and that needle selection
should be based on physician preference in conjunction The important factors in choosing an imaging modality
with consideration of the specific biopsy task at hand. for biopsy are lesion characteristics (e.g., size, location,
In general, initial samples are obtained for cytologic depth), ability to visualize the abnormality, and operator
analysis with fine-gauge (22-gauge) Chiba or spinal experience and preference. Generally, the shortest path
needles. If these needles do not yield satisfactory to the lesion is considered when planning the imaging
samples, a Franseen needle often yields cells for approach, with the possible exception of peripherally
cytologic study. Superficial lesions are easier to reach; located hypervascular hepatic lesions and when prepro-
deep-seated ones may require larger-gauge needles to cedure imaging demonstrates better tissue yield from a
provide sufficient stiffness to direct the needle accurately. different axis (e.g., elongated but thin lesion).
Noncutting Needles
Cutting Needles
END TYPE
Turner 45-degree tip
SIDE TYPE
Westcott Slotted outer cannula
A B
operator variability in experience and technique can The advent of three-dimensional sonography has
play a part in sonographically guided biopsies. aided percutaneous biopsy by precise delineation of
Specifically designed and somewhat costly reflective mass lesions and adjacent structures (e.g., blood vessels
needles are available. However, standard biopsy needles and bile ducts) in the anticipated needle pathway.12 It
are visualized adequately at real-time sonography, also has been useful in guiding transjugular liver proce-
particularly with gentle motion of the needle tip. Low- dures and regional tumor ablation procedures because
frequency transducers (e.g., 3.5-MHz sector probe) orthogonal images can be obtained in planes that are
are needed for deeper lesions. Higher-frequency trans- anatomically useful to the interventionalist performing
ducers (e.g., 7-MHz linear or phased-array probe) are the procedure. Three-dimensional sonography, how-
used for biopsy of superficial masses such as thyroid ever, has not gained significant popularity in most
nodules. Specifically designed probes for transvaginal practices.
and transrectal imaging have needle guides to facilitate
biopsy of pelvic lesions. Computed Tomography
The needle can be inserted perpendicular to the trans- CT is used for biopsy of smaller intraabdominal and
ducer, which may facilitate visualization by improved thoracic lesions not well visualized by ultrasound or
reflections from the needle shaft11 (Fig. 4-3). Alterna- fluoroscopy. The patient is first scanned in the antici-
tively, the needle can be inserted in close to the ultra- pated biopsy position (e.g., prone, supine, oblique) with
sound transducer. Ideally, the entire needle should be images obtained through the target area (Fig. 4-6). Intra-
visualized during passage through the tissues into venous contrast may be helpful in delineating vascular
the mass (Fig. 4-4). If the needle is not visible, misalign- structures, in determining the vascularity of the target
ment between the needle path and ultrasound beam is lesion, and for biopsy of lesions not well seen on unen-
occurring. A slight rocking motion (or panning) back hanced images (Fig. 4-7). A variety of devices is avail-
and forth of the ultrasound transducer may help visual- able to mark the skin during scanning and to determine
ize the needle. A gentle in-out motion of the needle or the needle insertion site and angle.
stylet may increase conspicuity of the needle tip as well. A vertical needle pathway is preferable because it
In every case, the needle tip should be documented as avoids the need for triangulation or accurate angle mea-
a discrete echogenic focus within the lesion in at least surements. The needle should be visualized in the axial
two views before biopsy (Fig. 4-5). plane during the biopsy. Occasionally, gantry angulation
Colinear
A
A B
FIGURE 4-5 Ultrasound-guided percutaneous biopsy of a hepatic mass. The patient had cryptogenic cirrhosis and an incidental
hypoechoic, 6-cm lesion in the medial segment of the left lobe. A, The sagittal image shows the lesion (straight arrows), pericardium
(curved arrows), and inferior vena cava (double arrows). B, Real-time imaging shows the brightly echogenic needle tip within the
lesion (arrow).
A B
C D
FIGURE 4-6 Technique for computed tomography (CT)-guided percutaneous biopsy. The patient had undergone resection for colon
carcinoma. Rising carcinoembryonic antigen titers were found later along with mediastinal lymphadenopathy on a CT scan. A, Using the
initial diagnostic CT scan as a guide, the patient is positioned in the scanner with a grid marker taped to the skin (arrows) near the anticipated
needle entry site. B, Scans are obtained through the lesion, and the table position that best shows the lesion is identified. Note the grid bars
on the skin overlying the mass. C, Cursors measure the distance between grid bars (F-B), which allows determination of the cephalocaudal
location of the lesion. The planned skin entry site is labeled A, and the depth of lesion is the distance from A to C. D, The needle is advanced
in stages as serial scans follow its progress into the lesion. The needle tip is seen as a beam-hardening artifact. In this case, no malignant tissue
was recovered.
4. PERCUTANEOUS BIOPSY 89
A B
may be helpful to visualize cranial-caudal angled ap- or that special needle holders be used. The technique
proaches (e.g., adrenal biopsy, transthoracic biopsy with also is useful to perform peripheral lesional biopsy
overlying ribs). when central necrosis is present. CT fluoroscopy is not
The advantages of CT include high-resolution image used universally, because some investigators are con-
quality and the ability to visualize all structures in cerned about added radiation exposure and conflicting
the path of the lesion including bowel. Disadvantages studies about reduced procedure times. CT fluoroscopy
include additional radiation exposure for the patient, has been used most often for transthoracic biopsy,
lack of real-time feedback during needle advancement for which high rates of technical success have been re-
and biopsy, and difficulty in using angled approaches ported with sensitivity ranging from 89% to 95% and
required for targeting abdominal masses high under the specificity of 100%.14 Several recent studies have shown
diaphragm. Spiral CT improves needle tip localization that using intermittent quick check CT fluoroscopy
because of minimal respiratory motion artifact and fast between needle advancements instead of continuous
scanning times. (near real-time) fluoroscopy can reduce radiation doses
CT fluoroscopy allows real-time monitoring of needle significantly.15,16
positioning during percutaneous biopsy. Since its intro-
duction in 1996, various studies have outlined advan- Magnetic Resonance Imaging
tages and disadvantages of this technique for biopsy Several investigators have described initial experiences
of various targets.13 Advantages of CT fluoroscopy over with MR-guided percutaneous biopsies. Potential advan-
conventional CT include the ability to time a patients tages include the ability to image lesions not readily
breathing to access moving lesions or to avoid ribs and seen by other modalities, multiplanar imaging capabil-
other overlying structures. CT fluoroscopy allows the ity, near real-time imaging during needle insertion, lack
needle and lesion to be visualized during sampling to be of ionizing radiation, and potential use of MR-guided
sure the needle tip is properly located within the lesion. tumor ablation in conjunction with biopsy.17 Disadvan-
Using CT fluoroscopy in near real-time imaging requires tages include the need for specially designed needles
either that the operators hands be in the radiation beam compatible with MR scanners, higher imaging costs, and
90 I. BASIC PRINCIPLES AND TECHNIQUES
special magnet configurations (i.e., open designs) to facili- oscillating and rotating motions of the needle hub while
tate needle insertion. 5 to 10 mL of continuous suction is applied with a 10-mL
Magnetic fieldbased electronic guidance systems are syringe connected by extension tubing. During needle
a special class of equipment that uses a low magnetic advancement and biopsy, the patient should suspend
field with position sensors on the patient fused with respiration to minimize inadvertent motion of the
previously obtained cross-sectional imaging to provide needle or target. With ultrasound, fluoroscopy, and CT
near real-time targeting.18,19 fluoroscopy, the position of the needle tip can be observed
Using a computer-calculated map, the operator can po- continuously during biopsy so that different sectors of
sition the needle based solely on the prior imaging or can the lesion are sampled to increase the diagnostic yield.
be coupled with real-time ultrasound or CT for true con- Before the needle is removed, the suction is released to
cordance. These systems can be useful in targeting lesions prevent the entire sample from being aspirated into the
that are only visible on contrast-enhanced CT images. tubing or syringe. Ideally, the biopsy is performed with
a cytopathologist present.
If the sample is predominantly composed of red
Sampling Technique (Online Case 45) blood cells, a better sample may be obtained with a
Most biopsies are performed with the patient in a supine smaller-gauge needle (e.g., 25-gauge). A nonaspiration
position, although prone and oblique positions can be technique also can be used in which the needle is ad-
used when necessary. With a few exceptions, the short- vanced and retracted through the lesion without suction.21
est path to the lesion is preferred. Hypervascular hepatic Large lesions with necrotic centers may require biopsy
lesions should be approached through a sizable paren- of peripheral tissue to make a diagnosis (Fig. 4-9).
chymal track to reduce hemorrhagic complications20
(Fig. 4-8). The likelihood of pneumothorax is reduced by Single-Needle Technique
minimizing the number of pleural surfaces crossed With the single-needle method, the needle is advanced
during chest and some abdominal biopsies. It is optimal into position, and its location is confirmed (Fig. 4-10). If
to avoid traversing lung, pleura, pancreas, gallbladder, the needle location is unsatisfactory, it is left in place to
dilated or obstructed biliary ducts, and bowel during guide placement of a second needle. Each biopsy sample
biopsy procedures. Small and large bowel can be crossed that is obtained requires a new needle be placed into the
safely with small-gauge needles if no other pathway is lesion, adding to the complexity of the case and in-
available. However, sampling of intraabdominal fluid creasing risks for complications such as bleeding. This
collections through bowel loops is not advisable. technique allows sampling of different regions of a
Usually it is best to start with smaller needles (e.g., mass, which may improve biopsy yield. This technique
22-gauge) that can serve as localizers for subsequent is very useful for biopsy of superficial lesions such as
needle placement. Sampling can be performed with or thyroid nodules.
without suction. Suctioning sample is obtained by small
Two-Needle Technique
With the two-needle method, a needle is placed initially
A just superficial to the lesion to serve as a guide for
B
subsequent needle passage and biopsy with a tandem or
coaxial technique (see Fig. 4-10). Precise needle place-
ment needs to be done only once. The coaxial method
is particularly useful with smaller or deep lesions that
are difficult to localize. It has the further advantage that
a single puncture of the visceral organ capsule (or
pleura) is made, regardless of the number of biopsy
needle passes that are made. A disadvantage of this
method is that the sampling path of the biopsy needle is
limited by the direction of the outer guiding needle.
Several different commercially available coaxial sets are
now available and are particularly useful for biopsy of
thoracic and deep abdominal lesions. Care should be
maintained when using different needles from different
vendors as slight size/length incompatibilities may
FIGURE 4-8 Biopsy of suspected hypervascular peripheral
hepatic lesions. Bleeding is more likely if the parenchymal track is
arise, making biopsy difficult or impossible.
short (A), With a tangential approach (B), a long parenchymal track Additional special equipment is available, such as
should tamponade bleeding. a modified coaxial system (e.g., 23-gauge needle with
4. PERCUTANEOUS BIOPSY 91
A B
FIGURE 4-9 Value of sampling multiple regions of a lesion during percutaneous biopsy. The patient had an epigastric mass, obstructive
jaundice, and ascending cholangitis. A, Computed tomography (CT) demonstrates a large pancreatic mass encasing the hepatic artery and
displacing the portal vein, with extension of the mass into the porta hepatis. The patient had undergone biliary stenting with nondiagnostic
bile duct brushings. Initial samples from a CT-guided biopsy (not shown) from the center of the lesion revealed only necrotic cells. B, Sampling
the periphery of the lesion revealed adenocarcinoma. The gallbladder contrast is residual from a recent endoscopic retrograde cholangiopan-
creatography.
FIGURE 4-10 Single- and double-needle techniques for percutaneous biopsy. Left, Single-needle technique. If the initial pass misses
the lesion, the needle (A) is used to redirect a second needle (B) into the lesion. With each attempt, a new needle is reinserted with imaging
guidance. Center, Two-needle technique. With the tandem method, a second needle (A) is slid alongside the landmark needle (B) and then
used to perform the biopsy. The original needle is left in place to guide subsequent needle insertions. Right, With the coaxial method, a larger
needle (18- or 19-gauge) is inserted just up to the mass. The biopsy is performed with a longer, smaller-gauge needle (22-gauge) inside the
outer guiding needle.
removable hub is used to guide a 19-gauge biopsy needles (e.g., 25-gauge) also limit the blood content of
needle), for additional cost. the aspirate.
A small amount of aspirated material first is placed
on a slide. The material is spread and then air-dried
Specimen Handling
or fixed in alcohol. Air-dried samples are stained
An optimal cytologic specimen consists of a small with Diff-Quik (Baxter Healthcare, McGraw Park, Ill.)
amount of soft or semiliquid material with minimal for prompt diagnosis. Larger tissue fragments or mate-
bloody contamination.22 Smears should be composed rial are placed in a tube or container of 10% neutral
of a thin layer of cells and fragments; blood dilutes and buffered formalin for processing as a cell block. This
obscures the diagnostic material. Clotting of the speci- step is particularly important when immunohistochemical
men can be minimized by expeditious sample prepa- staining is required for diagnosis. Occasionally, the core
ration and prerinsing the aspiration syringe and needle sample can be used to perform a touch preparation
with a small amount of heparinized saline. Small-gauge in which the core sample is smeared across a slide or
92 I. BASIC PRINCIPLES AND TECHNIQUES
multiple slides and then the core is placed in formalin, with suspected vascular lesions (e.g., arteriovenous
the touch preparations are then processed similarly as malformation, pulmonary varix) and Echinococcus cysts.
other cytologic samples.23 The remaining core sample is Relative contraindications to lung biopsy include severe
processed for histologic examination. Touch prep or obstructive pulmonary disease, moderate to severe pul-
core roll preparation has been shown to improve the monary hypertension, contralateral pneumonectomy,
diagnostic yield during the biopsy when compared with ventilator dependence, and inability to cooperate with
fine-needle aspiration (FNA) alone.23-25 In combination breathing instructions. These patients are at increased
with FNA, this allows for fewer passes to obtain a diag- risk of or are less able to tolerate pneumothorax after
nostic sample without significantly altering the histo- biopsy.
logic sample. The workup of pulmonary lesions varies significantly
among institutions with regard to the use of percuta-
neous needle biopsy or surgical resection for an SPN.
Care After Biopsy The probability that an SPN represents a primary lung
After the biopsy sample is obtained, imaging is per- tumor rather than a metastasis from a known malig-
formed to exclude potential complications (e.g., upright nancy depends largely on the primary tumor type
chest radiographs 1 and 4 hours after percutaneous (e.g., 1:1.2 for colon cancer, 3.3:1 for breast cancer, 3.3:1
chest biopsy or sonography of perihepatic spaces, for bladder cancer, and 8.3:1 for head and neck can-
paracolic gutters, and pelvis after percutaneous liver cers).26 The false-negative rate for needle biopsy in pa-
biopsy). The patient is monitored for 2 to 4 hours after tients with malignancy is relatively high (up to one third
the procedure while intravenous access is maintained, of procedures).28,29 The cases in which clinical suspicion
and vital signs are obtained frequently. If the patient of malignancy is high require repeat biopsy or close
has remained stable and no new clinical symptoms de- follow-up. In some centers, a potentially malignant SPN
velop (e.g., chest pain, shortness of breath, abdominal in a low-risk operative patient often is resected without
pain, distention), the patient is discharged home with a prior needle biopsy.
family member after the patient assessment of proce-
dure and anesthesia scoring system exceeds the thresh- Technique
old level. If vital signs are abnormal or symptoms CT is helpful in planning all chest biopsies. CT can
develop, additional imaging may be required to ex- identify the most accessible lung lesion or an extrapul-
clude a complication. monary mass that can be biopsied more safely (e.g., liver
or adrenal gland). CT also outlines bullae that should
be avoided to reduce the likelihood of postbiopsy pneu-
SPECIFIC APPLICATIONS mothorax.
Sonography can be used for some pleural or pleural-
Chest based masses. Fluoroscopy-guided chest biopsies are
greatly facilitated with the use of a C-arm (see Fig. 4-2).
Patient Selection The needle and hub are aligned with the lesion in one
Percutaneous chest biopsy is performed for evaluation view while the needle is placed initially through the
of nodules or masses in the lung, hilum, mediastinum, skin. The tube is then rotated into the orthogonal
pleura, and chest wall.26-28 In general, masses that in- projection as the needle is advanced to the proper
volve lobar or segmental bronchi on chest radiography depth within the lesion. Aspiration of material is per-
or CT suggest the presence of an endobronchial lesion, formed under direct fluoroscopic visualization, with
and these are best approached with bronchoscopy. On spot images documenting needle position in various
the other hand, peripherally located lesions are not that projections. The technique for CT biopsy is described
accessible with bronchoscopy and are easily reached above in the CT section. Anterior mediastinal masses
with percutaneous biopsy. The most common indication can be approached through the sternum30 (see Fig. 4-6).
for percutaneous chest biopsy is the diagnosis of a soli- With very large mediastinal masses a parasternal ap-
tary pulmonary nodule (SPN), which is a rounded, well- proach can be used, keeping in mind the course of the
defined mass of less than 3 cm that is largely surrounded internal mammary arteries (Fig. 4-11). Artificial widen-
by lung. Percutaneous biopsy, particularly core biopsy ing of the extrapleural (paravertebral or substernal)
in conjunction with FNA, has been advocated for diag- space by injection of saline has been used to facilitate
nosing pneumonia and diseases that mimic pneumonia biopsy of lesions located in the posterior or anterior
(i.e., bronchiolitis obliterans organizing pneumonia, mediastinum.31 An alternative approach to mediastinal
neoplasms [lymphoma, bronchoalveolar cell carcinoma], lesions avoids visceral pleural traversal by using an
eosinophilic pneumonia, vasculitis [Wegeners granulo- existing pleural effusion or an iatrogenically created
matosis]).27 Percutaneous biopsy should be strictly avoided pneumothorax.32
4. PERCUTANEOUS BIOPSY 93
A B
follow-up, with repeat imaging and possible repeat For chest tube placement, anterior access is gained
percutaneous biopsy. through the second intercostal space in the midclavicu-
lar line. A direct trocar technique is used to place an 8- to
Complications 10-French (Fr) chest tube if a large pneumothorax is
The most common complication of lung biopsy is pneu- present to expedite treatment. Smaller pneumothoraces
mothorax, which occurs in 10% to 35% of cases.28 The risk can be treated using the Seldinger method as well. Air is
of pneumothorax is increased with preexisting lung dis- removed by aspiration, Pleur-Evac device, or Heimlich
ease (smoking), smaller lesion size, no history of prior valve. Some operators clamp the tube (or place to water
thoracic surgery, and advanced age.35 Nearly all pneu- seal) soon after placement and remove it if the pneu-
mothoraces appear on the 1-hour postbiopsy chest film, mothorax does not recur soon thereafter. Otherwise,
and essentially all are detected on radiographs obtained patients are admitted overnight.
4 hours after biopsy. 36 Additional complications include pulmonary hemor-
Most cases can be managed conservatively; repeat rhage, hemothorax (Fig. 4-12), hemoptysis, malignant
films are obtained to document stability, reduction, or needle tract seeding, and systemic air embolism39,40
resolution of the pneumothorax. Treatment is required (Fig. 4-13). If significant pulmonary hemorrhage occurs,
for about 5% to 15% of patients, based on development the patient should be turned so that the biopsied side
of symptoms, an enlarging pneumothorax, or pneumo- is down, keeping the hemorrhage outside of the unaf-
thorax that occupies more than 25% of the hemithorax. fected healthy lung. Systemic air embolism is a rare
Some pneumothoraces respond to simple aspiration ("0.07%), potentially fatal complication. The formation
with a plastic cannula.37,38 In a minority of cases, how- of a communication between an airway and a pulmo-
ever, a chest drainage tube is required. nary vein is one assumed mechanism of air embolism
A B
A B
FIGURE 4-13 A 77-year-old woman with a long history of cigarette smoking and emphysema and on home oxygen use was found
to have a left lower lobe pulmonary nodule. She was referred for percutaneous lung biopsy. A, Computed tomography (CT) image during
the biopsy, performed with the patient in a prone position, shows the needle in the lesion with pulmonary hemorrhage extending
anteriorly from the lesion. B, The patient had an uncontrolled episode of coughing during which air was aspirated into the needle. She had
a grand mal seizure. A repeat CT scan of the chest demonstrates air within the thoracic aorta (arrow), intercostal, and spinal arteries. She
responded to supportive measures and was found to have a lung adenocarcinoma, which was treated with radiation therapy (she was not
a surgical candidate).
Complications
The major complications of percutaneous liver biopsy
are bleeding, pneumothorax, malignant needle track
seeding, and infection. Although rare, fatal hemorrhage
can result, particularly after biopsy of a hemangioma or
hypervascular neoplasm. Hemorrhagic complications
from liver biopsy of diffuse liver diseases are less com-
mon than with biopsy of malignant lesions. Bleeding
usually occurs within several hours of the procedure
and often can be managed conservatively.48 Hemorrhage
may occur into the peritoneum or into the biliary system
(i.e., hemobilia). Less than 5% of outpatient liver biopsy
patients requires admission. At Doppler sonography,
a patent track sign after liver biopsy (particularly if
persistent for more than 5 minutes) strongly predicts
postbiopsy bleeding.49
FIGURE 4-14 Effect of colonic position on percutaneous liver The most common signs of significant bleeding are
biopsy. The initial biopsy to exclude hemochromatosis was abdominal or shoulder pain and hemodynamic instabil-
performed without imaging guidance and was nondiagnostic. The
proximal portion of the right colon is interposed between the right
ity. When clinical suspicion arises, serial hematocrits
lobe of the liver and the hemidiaphragm. Biopsy through this route and CT or ultrasound imaging should be obtained.
is relatively unsafe. Suspicion for hemobilia should be raised if clinical
4. PERCUTANEOUS BIOPSY 97
A B C
D E
FIGURE 4-15 A 67-year-old man with a history of colorectal cancer was found to have a lesion in the left lobe of the liver during follow-up
imaging. Axial T1- and T2-weighted and coronal T1 MR images of the liver (A, B, and C) were thought to be atypical for hemangioma, and
biopsy was suggested. Computed tomography (CT) images in arterial and delayed phases confirm the CT findings (D and E). A biopsy was
performed with ultrasound and the diagnosis was hemangioma. There was no postbiopsy bleeding.
symptoms are present, but no definite hemorrhage is adenomas can be diagnosed confidently by CT (noncon-
noted on imaging. Subtle findings such as high attenu- trast CT with threshold values to detect low attenuation or
ating material in the gallbladder on CT is also important contrast washout methods) or chemical shift MRI without
for diagnosis. In patients who continue to bleed, angiog- the need for tissue sampling. Application of these cross-
raphy and transcatheter embolization may be required sectional methods has reduced the number of adrenal
to control bleeding. Needle track seeding is less frequent biopsies yielding benign diagnoses to less than 12% in
than with biopsy of the pancreas. Fatal carcinoid crisis patients with extraadrenal malignancies.52 When adrenal
has been reported after biopsy of liver metastases.50 masses larger than 1 cm are detected in patients under-
going imaging procedures for nonadrenal problems, these
Adrenal Gland (Online Case 69) lesions are called adrenal incidentalomas.53 Guidelines
have been published to help in workup of these lesions.54,55
Patient Selection Functioning cortical adenomas and pheochromocytomas
Percutaneous biopsy is used for diagnosing focal lesions are best characterized by means of biochemical assays. All
of the adrenal gland. The most common adrenal masses hormonally active tumors causing Conn syndrome (aldo-
are nonfunctioning adenomas and metastases51 (Box 4-2). sterone hypersecretion) are resected after confirmation
Adrenal adenomas are seen in as many as 5% of patients by adrenal vein sampling (see Chapter 13). Inactive tumors
undergoing CT for unrelated reasons. In an asymptomatic are resected based on size, imaging characteristics, and
patient with an adrenal mass, the size of the mass and the interval growth. Percutaneous biopsy of these inciden-
presence or absence of a primary malignancy must be talomas is generally not warranted.
considered in determining the need for biopsy. When
adrenal lesions are larger than 3 cm, the likelihood of ma- Technique
lignancy is significant. Even in patients with a known Adrenal masses often are best approached from the
primary and an adrenal lesion, the likelihood of a positive back, respecting the location of pleural reflections. Other
biopsy is only about 50%. In some cases, nonfunctioning routes include a transhepatic approach for right-sided
98 I. BASIC PRINCIPLES AND TECHNIQUES
19-gauge) and when the lesion is located in the body or tail refinement of local ablative techniques and nephron
of the gland.59 In addition to standard cytologic evaluation sparing surgery.64
of tissue, fluid analysis for viscosity, enzymes, and tumor
markers may be valuable for cystic lesions.60 Technique
Complications develop after approximately 3% of Biopsy of focal renal masses is usually performed with
procedures and include hemorrhage, pancreatitis, and ultrasound guidance.63 CT is required when the mass is
pancreatic duct fistulas. Pancreatitis may be more com- difficult to visualize with sonography (Fig. 4-16). A pos-
mon after biopsy of a normal gland.61 Because rapid in- terior approach is used.
traabdominal spread of disease has been described after Biopsy for CKD and transplantation complications
intraoperative biopsy of pancreatic tumors, some sur- usually is performed with ultrasound guidance. Bi-
geons believe that percutaneous biopsy should be opsy of the lower pole is preferred to avoid vessels
avoided if curative resection is planned. Track seeding in the renal hilum or possible injury to the liver or
from needle biopsy has been reported, but it is rare.62 spleen. Large-core samples (with 16- to 18-gauge usu-
ally automated devices) are required to obtain the 5 to
Kidney 10 glomeruli needed for diagnosis.65-67 Transjugular
renal biopsy can be applied in patients at high risk for
Patient Selection bleeding complications.68
Renal disorders may be divided into diffuse processes
that produce chronic kidney disease (CKD) and focal Results and Complications
mass lesions.63 Large-core biopsy for CKD often is Using 18-gauge needles, a diagnosis is established in
performed by a nephrologist, with limited imaging 85% to 95% of patients with chronic kidney disease.63
guidance. Occasionally, a radiologist is asked to per-
form such a biopsy when the nephrologist is unable to
obtain adequate material. Percutaneous kidney biopsy
by an interventional radiologist has several established
indications (Box 4-4).
The expanded role of percutaneous biopsy of small
renal masses has been influenced by advances in cytol-
ogy, immunocytochemistry, and cytogenetics and by
BOX 4-4
I N D I C AT I O N S F O R A
KIDNEY BIOPSY
Established
Chronic kidney disease when imaging is difficult
(e.g., obese patients, atrophic kidneys) or initial
biopsy is inadequate
Focal renal mass in a patient with underlying
malignancy
Focal renal mass in a nonoperative patient
Focal renal mass in a patient with fever of
unknown origin
B
Emerging
FIGURE 4-16 Computed tomography (CT)-guided kidney
Small (#3 cm) solid renal mass biopsy. A, CT in the prone position shows a hyperdense right renal
Renal mass being considered for percutaneous mass (arrow) in a patient with cutaneous melanoma. Grid bars are
ablation taped to the skin over the lesion. B, Three passes were made with
Indeterminant cystic renal mass 22-gauge Chiba needles. The outer needles missed the lesion but
were left in place to assist with accurate placement of the third
needle just beyond the mass.
100 I. BASIC PRINCIPLES AND TECHNIQUES
Complications follow about 1% to 6% of percutane- suspected, core biopsy may be required for immunocy-
ous renal biopsies.65,69 After biopsy, small arteriovenous tochemical studies, flow cytometry, cytogenetic analysis,
fistulas and pseudoaneurysms are relatively common. or molecular studies, and a posterior route is prefera-
Many of these close spontaneously without the need ble. Biopsies of almost all retroperitoneal masses are
for treatment. Significant hematomas with falling hema- conducted under CT or ultrasound guidance.
tocrit levels and persistent gross hematuria are uncom- Metastatic lymphadenopathy from tumors of the gastro-
mon. A prospective study of biopsies for chronic kidney intestinal and genitourinary tracts can be diagnosed
disease in 471 patients found that 161 patients (34.1%) in about 65% to 90% of cases.72 Historically, the diagnos-
experienced postbiopsy bleeding (33.3% hematomas, tic accuracy of percutaneous biopsy in patients with
0.4% gross hematuria, 0.4% arteriovenous fistula).70 lymphoma is about 20% lower than for nonlymphoma-
Major complications occurred in six patients (1.2%), with tous retroperitoneal lesions. Later series reported higher
two requiring blood transfusions, three requiring an- success rates.73 A negative percutaneous biopsy cannot
giograms, and one requiring nephrectomy. There were entirely exclude a malignant process. If several properly
no deaths. Angiographic evaluation and transcatheter performed biopsy attempts fail to provide a cytologic
embolization are required occasionally for treatment of or histologic diagnosis, an excisional biopsy may be
bleeding that does not stop with conservative measures. required. The yield for rare malignant forms of retro-
peritoneal fibrosis is relatively low, and surgical biopsy
Other Abdominal and Pelvic Sites often is needed to identify the diffusely dispersed malig-
nant cells that are characteristic of this condition.74
(Online Case 30)
Peritoneal soft tissue masses and mesenteric lymphade-
Splenic biopsy is rarely performed because focal masses nopathy are amenable to percutaneous biopsy tech-
are uncommon. Although there is particular concern niques. Ultrasound guidance greatly facilitates biopsy
about splenic hemorrhage, biopsy with 20- to 22-gauge of these entities.75 Such lesions often are better visu-
Chiba or spinal needles is relatively safe.71 Biopsy may be alized by external compression with the ultrasound
performed with CT or ultrasound guidance. The largest, transducer to displace bowel loops overlying the mass.
most superficial lesion usually is chosen; the splenic Deeper lesions can be approached with CT (Fig. 4-17).
hilum, colon, kidney, lung, and pleura should be avoided. Biopsy of peritoneal masses poses a small risk of ileus
Hemorrhage is the most common complication (typically or peritonitis ("1%).
0 to 1.5% but as high as 10% of patients); other com- Pelvic lymphadenopathy or soft tissue masses can be
plications include pneumothorax, pleural effusion, and approached through transperitoneal (anterior or trans-
colonic injury. gluteal), extraperitoneal, transvaginal, or transrectal
Retroperitoneal masses can be approached from an routes. The transvaginal approach is useful especially
anterior or posterior route. The major disadvantage of for biopsy of primary or recurrent adnexal or ovarian
the anterior approach is that bowel may be traversed. masses.76 For diagnosis of metastatic prostate cancer,
However, this route is reasonable if cytologic analysis CT-guided biopsy with thin section CT is accurate in up
using small-caliber needles is sufficient. If lymphoma is to 97% of cases.77
A B
FIGURE 4-17 An 80-year-old man with abdominal pain was found to have lymphadenopathy that slowly enlarged on serial computed
tomography (CT) scans of the abdomen. A and B, CT-guided biopsy shows percutaneous biopsy performed around surrounding adjacent
bowel loops.
4. PERCUTANEOUS BIOPSY 101
Presacral masses in patients who have undergone cases of thyroid cancer were expected to be diagnosed in
abdominoperineal resection can be evaluated with per- the United States in 2009, with 163 deaths expected to be
cutaneous biopsy. Although such masses are not uncom- attributable to thyroid cancer.79 Risk factors for thyroid
mon in postoperative patients, a rising carcinoembry- cancer include family history of thyroid malignancy, a
onic antigen level or asymmetric thickening of the history of prior head and neck radiation, age younger
presacral space may indicate recurrence. These lesions than 30 years or older than 60 years, and patients with
are accessed easily through a transgluteal approach, tak- multiple endocrine neoplasia type 2.80
ing care to avoid the sciatic nerve running in the anterior Clearly, there is a need to differentiate the uncommon
third of the greater sciatic notch. but important thyroid carcinoma from the common,
Percutaneous biopsy techniques also can be applied insignificant thyroid nodule (Table 4-2). However, there
to a variety of uncommon intraabdominal or intrapelvic is much overlap in the ultrasonographic appearance of
lesions, including omental cakes, mesenteric root masses, benign and malignant nodules81 (Fig. 4-19). Ultrasono-
and mucosal lesions of the stomach, bile ducts, or uri- graphic features suggesting malignancy include a solid,
nary tract (Fig. 4-18). hypoechoic nodule; punctate calcifications; a poorly de-
fined, indistinct, or blurred lesional margin; direct inva-
Thyroid (Online Case 40) sion of the nodule through the thyroid capsule; and
central rather than peripheral vascularity within the
Patient Selection lesion.78,82 Hyperechoic nodules, cystic nodules, and
Thyroid nodules are the most common pathologic find- nodules with complete halos are typically benign. Size
ing in the thyroid gland.78 In general, about 4% to 7% of a nodule is not a reliable indicator of the benign or
of the population of the United States has clinically pal- malignant nature of thyroid nodules. In most cases, FNA
pable thyroid nodules. The incidence of thyroid nodules biopsy of the thyroid can differentiate benign nodules
increases with age and is more prevalent in females from thyroid neoplasms, which has reduced the num-
of all ages. Autopsy studies indicate that clinical exami- ber of patients undergoing surgical excision of benign
nation has limited ability to detect nodules, particularly nodules. Several criteria are available for determining
smaller nodules and nodules situated deeper within
the thyroid gland. Several studies also have shown that
ultrasound reveals occult nodules in about 50% patients TABLE 4-2 Differential Diagnosis of Thyroid Nodules
who have a normal thyroid gland on physical examina-
tion.78 Many nodules come to attention as a result Benign Malignant
of other diagnostic imaging studies, such as chest CT, Hyperplastic nodule; Primary (papillary, follicular,
carotid sonography, and cervical spine MRI. Less than adenomatous nodule Hrthle, medullary, anaplastic)
5% of thyroid nodules are malignant. Follicular or Hrthle cell Metastases (renal, breast,
Thyroid cancer is the most common malignancy of adenoma melanoma)
Lymphocytic thyroiditis Lymphoma
the endocrine system, with more than 80% representing
Cyst (pure cyst is rare: "3%)
papillary thyroid carcinoma. More than 37,000 new
A B
FIGURE 4-18 Percutaneous gastric wall biopsy. The patient had multiple negative endoscopic gastric biopsies. The upper gastrointestinal
series had a linitis plastica appearance. A, Computed tomography scan shows diffuse gastric wall thickening (arrows). B, The biopsy under
sonographic guidance (arrow) revealed signet cellpositive gastric carcinoma.
102 I. BASIC PRINCIPLES AND TECHNIQUES
A B
whether a nodule should be biopsied. The three most is performed by connecting a 10-mL syringe to the
popular ones are the Kim criteria, American Association 25-gauge needle with connecting tubing. A similar
of Clinical Endocrinologists criteria, and the Society of biopsy motion is used while suction is applied with
Radiologists in Ultrasound criteria.80,83,84 One recent 1- to 2-mL aspiration of the syringe. The samples are
study suggests that the former two protocols are more placed onto a slide. If the gross appearance of the
accurate than the latter one.85 smear appears scant, additional passes (up to 6 or 8)
should be made, assessing different parts of the nodule
Technique to increase the biopsy yield. Some investigators have
The patient lies supine on a stretcher. Neck extension used 20- and 22-gauge cutting-needle biopsy guns for
aids in visualizing the thyroid gland, which is obtained lesions that are hypocellular, particularly if the lesion is
by placing a rolled towel behind the patients lower larger than 1 cm.
neck. Sonography is performed with a high-frequency
(8 to 15 MHz) linear array transducer to localize the Results and Complications
nodule to be biopsied. A sterile ultrasound probe is set Reported rates of diagnostic accuracy range from 85%
up and sterile gel placed on the patients neck. After to 95%.78,86 The use of thyroid FNA biopsy has been
local anesthesia is applied, a 3-cm, 25-gauge needle is shown to reduce the number of thyroidectomies by ap-
then placed into the lesion with continuous sonographic proximately 50%, roughly double the surgical yield of
visualization. Specimens may be obtained by either a carcinoma, and reduce the overall cost of medical care in
nonaspiration or an aspiration technique. The patient these patients by 25%. The yield from biopsy of cystic
is instructed to refrain from talking, breathing, or swal- thyroid nodules is lower, with about 39% of cases yield-
lowing while the biopsy is being performed. With the ing unsatisfactory cytologic results.87 The appropriate
nonaspiration technique, cells are pulled into the needle action following a nondiagnostic biopsy is controversial.
by capillary effect. With this technique, the biopsy is Follow-up is at the discretion of the referring physician.
performed by moving the needle back and forth vigor- Management options include repeat biopsy, surgery, or
ously through the nodule until bloody material is seen at close imaging surveillance. One study found that repeat
the hub of the needle. The suction aspiration technique biopsy of such cases revealed malignant lesions in about
4. PERCUTANEOUS BIOPSY 103
half of the cases.88 These authors suggested that opera- been inserted so that the lesion is accessed. Repeat biop-
tors wait at least 3 months before repeating the biopsy sies with this technique require additional needles be-
because needle-induced reparative cellular atypia com- cause this approach is coaxial. A second method em-
plicates subsequent cytologic diagnosis. The complication ploys a coaxial technique with custom bent thin-walled
rate from thyroid biopsy is less than 1% and most relate 19-gauge needles that are then inserted with CT or MR
to small hematomas.80 fluoroscopy. A 21-gauge needle is advanced through
the arc-shaped, outer 19-gauge needle to perform the
biopsy. A variation is to use a straight 18-gauge needle
METHODS TO REACH through which a curved 22-gauge needle is advanced.14
INACCESSIBLE LESIONS
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Radiology 1997;203(1):1. sonography-guided biopsy of the liver in the presence of ascites:
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AJR Am J Roentgenol 1995;165(5):1277. transpulmonary CT-guided liver biopsy: a safe and technically
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C H A P T E R
5
Transcatheter Fluid Drainage
Ajit V. Nair, Horacio R. DAgostino
106
5. TRANSCATHETER FLUID DRAINAGE 107
confirm the viability of the chosen access route. The pa- (e.g., color, viscosity, turbidity, odor), and the sample is
tient is then prepped and draped in a sterile fashion, sent for Gram stain, culture, sensitivity, cytology
and local anesthetic is administered to the access site. (if there is concern for malignancy), and other tests as
Local anesthesia should be generously applied to both necessary. If catheter placement is to follow, only a
the skin surface and the deep tissues, particularly at small fluid sample (!5 mL) is removed initially,
innervated surfaces such as the peritoneum, pleura, or because decompression of the collection may compli-
organ capsule (i.e., liver, kidney). Good local anesthesia cate or preclude tube insertion. Conversely, complete
maximizes patient comfort and minimizes the need for aspiration should be performed if imaging shows the
intravenous conscious sedation. collection to be too small for drainage catheter place-
Needle selection is based on the objective of the pro- ment, thus assisting in its resolution. Dry aspiration
cedure (i.e., aspiration vs. drainage catheter placement) from an 18-gauge needle well positioned within the
and location of the collection to be drained. Generally, collection may indicate that the lesion is either very
small-caliber needles (18- to 22-gauge) are chosen with viscous or not drainable. Often, the ability to pass a
a length sufficient to reach the collection. Eighteen- guidewire, and ultimately a catheter, into the collection
gauge Chiba and Hawkins needles have thinner walls determines whether drainage is possible. If not, the
than comparable spinal needles and are preferable tissue may then be biopsied with specimens sent for
when drain placement is desired, because they accept a cytology and microbiology.
0.035-inch guidewire. Conversion of an aspiration procedure to drainage
After the application of local anesthesia, a scalpel is catheter placement is based on multiple factors. One
used to puncture the skin and underlying fascia to allow small, retrospective study found that more than half of
for ease of needle and possible catheter insertion. This all sterile pancreatic fluid collections found in acute pan-
maneuver is particularly useful when using a sono- creatitis treated with long-term catheter drainage under-
graphic needle guide for real-time imaging. went bacterial colonization.8 Thus, by convention, sterile
Sonography and fluoroscopy allow for needle localiza- pleural effusions or ascites are often treated with thera-
tion under direct imaging guidance (Fig. 5-1). Imaging peutic aspiration alone, because placement of an in-
under CT is performed intermittently during needle inser- dwelling drainage catheter can promote infection of
tion, advancing the needle before acquiring a limited CT these collections. The same is true for fluid collections
slice to determine needle location and trajectory. Successful elsewhere, such as joint effusions. Infected collections
puncture of the collection, wire localization, and drainage often require placement of a drainage catheter; however,
placement are all confirmed by CT (Fig. 5-2). aspiration may be performed on collections that are too
small for placement of a drainage catheter. Drains are
placed for symptomatic collections that recur after
DIAGNOSTIC ASPIRATION therapeutic aspiration, such as cysts and pseudocysts.
One-step needle aspiration without catheter insertion
Diagnostic aspiration of fluid collections is a useful tool may be performed in certain locations without expected
for both diagnosis and treatment. It can be used to ob- communication with the gastrointestinal, biliary, or uri-
tain a sample to determine the transudative or exudative nary tracts. This approach has reported success rates up
nature of a collection, can assist in the tailoring of the to 90% in selected cases.6,9-12
appropriate antibiotic regimen, and helps determine the
appropriate drainage catheter. Aspiration may be per-
formed as a stand-alone procedure or may precede drain CATHETER INSERTION
placement, because aspiration is the first step in the
placement of a percutaneous drain. Choice of catheter size and type is determined by the
As noted in the previous section, small-caliber needles type and character of the fluid to be drained. Air and
(18- to 22-gauge) are typically selected for aspiration. thin fluids are drained with 8- and 10-Fr catheters. Vis-
Alternatively, an over-the-needle catheter system may be cous fluids and fluids containing particulates require
employed, such as the Yueh or OneStep catheter systems. larger drainage catheters ranging from 12- to 26-Fr. Most
These are 4- and 5-French (Fr) catheters that slide into po- drainage catheters have an inner retention mechanism,
sition over the introducer needle, much like a peripheral such as the locking pigtail (Cope loop) or Malecot drains
intravenous catheter. Such systems are useful for aspira- (Fig. 5-4).
tion of simple fluid collections of some volume, in which Drainage catheters may be placed using different
a drainage catheter placement is not indicated, such as a techniques: direct trocar, tandem-trocar, and Seldinger.
therapeutic thoracentesis or paracentesis (Fig. 5-3). The direct trocar technique can be safely performed on
Aspiration of fluid confirms needle location in the large superficial collections. After application of local
collection. Fluid characteristics are assessed qualitatively anesthesia, the skin is incised with a scalpel and the
108 I. BASIC PRINCIPLES AND TECHNIQUES
A B
C D E
F G
5. TRANSCATHETER FLUID DRAINAGE 109
A B
C D
FIGURE 5-2 Computed tomography (CT)-guided drainage of right lower quadrant abscess. A, CT shows collection of fluid and gas in the
right lower quadrant consistent with abscess (arrows). Note radiopaque marking grid overlying the anterior surface of the right lower quad-
rant. B, Access needle is directed into the collection under intermittent CT guidance. C, A guidewire is advanced and curled in the collection.
D, Using Seldinger technique, a pigtail drainage catheter is placed over the wire.
A B
incision spread with a Kelly clamp. The catheter is di- catheter shaft. The catheter, with the metal cannula and
rectly inserted into the collection with the inner cannula stylet, is placed in the skin hole next to the previously
and stylet. The stylet is then removed and the cannula is inserted needle and advanced into the collection under
aspirated. The catheter is then inserted over the cannula imaging guidance. The stylet is removed, and material
or guidewire. can be aspirated. A 0.035-inch guidewire is then ad-
The tandem-trocar technique is a variation of the trocar vanced through the cannula, and the catheter is inserted
technique, in which the distance between the skin and over the cannula and guidewire into the collection. Use
collection is measured by imaging and marked on the of the guidewire decreases the risk of perforation of the
110 I. BASIC PRINCIPLES AND TECHNIQUES
A B
C D
FIGURE 5-5 Ultrasound-guided placement of a drainage catheter in a right lower quadrant abscess using Seldinger technique. A, Computed
tomography demonstrates right lower quadrant fluid collection. B, Ultrasound-guided access into the collection. The guidewire has been placed
through the needle into the collection (arrows). C, Ultrasound shows the pigtail drain inside the collection. D, Fluoroscopic image demonstrates
the location of the catheter within the right lower quadrant.
5. TRANSCATHETER FLUID DRAINAGE 111
A B C
FIGURE 5-6 Dry-suction water-seal chest drain. A, This drainage system contains a graduated chamber for collecting fluid, a water seal
chamber to evaluate for air leak, and a pressure regulator. B, The water-seal chamber is filled with saline. This connection is then attached to
suction. Tubing to the right is attached to the chest tube. C, Water-seal chamber. Air bubbles in this chamber indicate an air leak within the
chest tube system.
112 I. BASIC PRINCIPLES AND TECHNIQUES
TABLE 5-1 Algorithm for Percutaneous Fluid Drain The success rate of PFD combined with antibiotics and
Management nutritional support is about 90% for simple collections
CLINICAL STATUS
(cysts, unilocular abscesses). The cure rate drops to 70%
for complex collections such as infected hematomas,
Improved Stable/Declined multilocular abscesses, abscesses complicated by bowel
Decreased drainage Remove catheter Reimage and reassess fistula, pancreatic abscesses, and infected necrotic pan-
output creatic collections.15,16 Drainage failures often are attrib-
Increased or stable Sinogram to evaluate Leave catheter in uted to residual undrained collections, premature tube
output for fistula place and continue
removal, or inadequate position (or number) of catheters.
maintenance
However, even when PFD is not completely curative, it
5. TRANSCATHETER FLUID DRAINAGE 113
B C
FIGURE 5-7 Drain catheter reposition after drain output decreased. A, Computed tomography (CT) scan shows drainage catheter pigtail no
longer in the largest portion of the collection (arrow), after having successfully drained the material surrounding the tube. B, Catheter sinogram
under fluoroscopy shows main portion of the abscess cavity beyond the pigtail loop. The contrast-filled sac provides a target for repositioning
the tube. C, Catheter repositioned into the remaining collection. The former catheter was removed over a stiff guidewire, which was advanced
into the larger collection for drain replacement.
often converts an emergent operation (with its attendant removed. A Foley catheter is placed (if not already pres-
risks) to an elective procedure or obviates the need for a ent) to ensure good bladder drainage. The Foley catheter
two-stage operation (e.g., diverting colostomy). is left in place for 5 to 7 days to allow healing of the per-
The major complications of PFD are bleeding, bowel foration. The catheter then is clamped for 4 hours and
or bladder perforation, and sepsis. Hemorrhage is removed if no urine leak is evident.
more likely to occur in a patient with an uncorrected
coagulopathy or when a suboptimal access route was
used for catheter insertion. Inadvertent bowel perfora- SPECIFIC APPLICATIONS
tion may take place when bowel motility is impaired
by adhesions or ileus. If a loop of bowel is traversed en
Chest
route to a fluid collection, a second catheter is placed
in the collection. The first catheter is withdrawn until PFD is indicated for treatment of pneumothorax, empy-
its tip is in the bowel lumen. This enterostomy catheter ema, malignant pleural effusion, pericardial effusion,
is removed when a mature track has formed. If an lung abscess and mediastinal abscess.17 Imaging guid-
abnormally distended loop of bowel is mistaken for an ance may be provided by sonography, fluoroscopy, or
abscess, aspiration yields yellow-green fluid that con- CT, with sonographic guidance being the most common.
tains bubbles and is not foul smelling. In this situation, Typically, catheters placed in the chest cavity are
the catheter should not be removed but rather kept in connected to a water-seal drainage device.
place for 10 to 15 days until a track has formed. The Bleeding risk is posed by the intercostal and internal
catheter then can be removed safely, and the track mammary arteries. Transection of the intercostal vessels
closes spontaneously. is largely avoided by inserting needles and catheters
Perforation of the bladder may occur while draining over the upper border of the ribs. The internal mam-
lower abdomen fluid collections, regardless of the access mary vessels are avoided by placement of needles and
route. Foley catheter insertion in the bladder before the catheters at least 5 cm lateral to the sternal margins, or
procedure may avoid this complication. On recognition of by direct visualization of these vessels during placement
bladder perforation by a drainage catheter, the catheter is under CT or sonography.
114 I. BASIC PRINCIPLES AND TECHNIQUES
Pneumothorax has been treated traditionally by surgical complete evacuation of the pneumothorax, in that
large-bore chest tube placement, but is very amenable to sections of the lesion may be walled off from the com-
small-bore catheter placement by the interventionalist. partment containing the chest tube. Under CT guidance,
Additionally, pneumothorax is a common complication these loculations can be identified and a chest tube
of percutaneous lung biopsy and should be managed placed through the septation; alternatively, individual
by the interventionalist, as its treatment has many catheters may be placed in each loculated compartment.
aspects in common with abscess drainage.18 Indications Needle, wire, and catheter placement is similar to that
for chest tube placement include large-volume pneumo- of free-flowing pneumothoraces, except intermittent
thorax ("30% of the hemithorax), the appearance CT imaging is performed to guide needle and tube
of symptoms (e.g., dyspnea, decrease in blood-oxygen placement.
saturation), or need to re-expand the lung to continue Empyema is an infected pleural collection usually
with lung biopsy. caused by pneumonia, bronchiectasis, or trauma. Empy-
In free-flowing pneumothoraces, catheter insertion is emas evolve in the following three stages19:
performed using anatomic landmarks or under fluoro-
Acute (exudative) phase, indicated by the pres-
scopic guidance. With the patient supine, the anterior
ence of a nonviscous, nonloculated effusion
chest wall is sterilized. Local anesthesia is provided at
Subacute phase, in which the fluid is fibrinous or
the skin level as well as at the pleural surface; if ade-
purulent and the cavity may have loculations
quate local anesthesia at the pleural interface is attained,
Chronic (organizing) phase, when there is organi-
catheter insertion can be virtually painless for the pa-
zation of the exudate with adhesion of the
tient. An 18-gauge needle is inserted between the second
visceral and parietal pleurae (i.e., pleural peel)
and third anterior ribs in the midclavicular line with
suction applied through a syringe until air is aspirated. The diagnosis is made at the time of aspiration by the
An alternative site in women and in men with bulky presence of gross pus, fluid pH 7.2 or lower, bacteria
pectoralis muscles is the fourth or fifth intercostal space identified by Gram stain, or a fluid glucose less than
at the anterior axillary line. A stiff 0.035-inch guidewire 40 mg/dL.20,21 CT diagnosis may be made by identifica-
is inserted and angled toward the apex of the hemitho- tion of the split pleura sign, in which the visceral and
rax. An 8-Fr catheter is then inserted over the wire with parietal pleura are thickened on contrast-enhanced CT
the pigtail formed at the apex of the pleural space. The and divided by pleural fluid.22 Acute and subacute
tube is then connected to a Heimlich valve or a water- empyema is treated successfully by PFD in greater than
seal drainage device immediately after placement and is 80% of cases; chronic empyemas respond much less
left connected to drainage for at least 12 hours. The cath- well.23,24 Catheters are typically placed using ultrasound
eter can be removed when the lung remains expanded and fluoroscopy after diagnostic aspiration; CT may be
on a follow-up chest radiograph obtained 2 hours after used to access loculated collections, which may require
clamping the tube (Fig. 5-8). multiple tubes. Fluid viscosity is used to determine the
Loculated pneumothoraces may require placement of a size of the catheter placed, usually ranging from 12 to
chest tube using CT guidance. Loculations may prevent 24 Fr. The catheter is connected to a water-seal drainage
A B
FIGURE 5-8 Postbiopsy pneumothorax tube placement. A, The patient developed a large, symptomatic left pneumothorax after percutane-
ous biopsy of a lung mass with a 22-gauge Chiba needle. B, The pneumothorax was treated by evacuation through a pigtail catheter placed in
the second intercostal space.
5. TRANSCATHETER FLUID DRAINAGE 115
device and continuous low wall suction after insertion. Placement of these catheters involves traditional percuta-
Intrapleural t-PA instillation is necessary to improve neous access of the fluid in the pleural space, typically
drainage, particularly in fibrinous collections.25 A 2- to caudally within the chest. The catheter is then tunneled
4-mg dose of t-PA in 10 to 20 mL of saline, depending on under the skin between the ribs near the midclavicular
the size of the tube and collection, is administered and line to the access site, where it is placed into the pleural
the tube is clamped for several hours before drainage is space through a peel-away sheath. The catheter is acces-
resumed. This step can be performed every 8 hours and sible to the patient for periodic drainage, with the exposed
may be done for several days to ensure resolution of the portion distal to the site where it enters the pleural space.
collection. Empyema catheters are removed when there Infrequently, these catheters are complicated by leakage,
is improvement in clinical and laboratory parameters, migration, loculation of the effusion, or infection.
no sign of air leak to indicate a bronchocutaneous Lung abscess is an infected collection of the lung paren-
fistula, and drainage of less than 10 mL/day. chyma. Primary abscesses usually are the consequence of
Malignant pleural effusions tend to recur rapidly after aspiration and are caused by anaerobic bacteria. Secondary
therapeutic thoracentesis. Closure of the pleural cavity abscesses arise from an adjacent infection or hematoge-
(pleurodesis) with a sclerosing agent (e.g., tetracycline, nous spread (e.g., pneumonia, lung cyst, septic emboli).
doxycycline, talc, diluted sodium hydroxide, bleomycin) About 90% of lung abscesses respond to antibiotics, pos-
is an effective way to prevent recurrent effusions in more tural drainage, and bronchoscopic lavage. Those that do
than 80% of patients.26 Before sclerosis, the pleural fluid is not resolve with more conservative measures require
drained completely. Usually, several sessions of sclerosis percutaneous drainage.28-31 The procedure is performed
are needed to achieve fusion of the pleural surfaces. More with fluoroscopic or CT guidance (Fig. 5-9). A catheter
recently, placement of tunneled pleural drains (Pleur X pathway through abnormal lung is preferred to avoid
catheters) has gained favor in the treatment of malignant pneumothorax and collapse of the healthy lung. Rarely,
pleural effusions in terminal patients, particularly those this is not possible and normal lung must be traversed
who failed pleurodesis.27 Such catheters allow for inter- by the drainage catheter. The patient is positioned to
mittent drainage to be performed by the patient or care- keep the opposite hemithorax nondependent to avoid
taker, with a theoretical decrease in the risk of infection aspiration of the abscess fluid into the normal lung. Cath-
or pneumothorax formation in the outpatient setting. eter insertion in a lung abscess establishes a controlled
A B
C
116 I. BASIC PRINCIPLES AND TECHNIQUES
bronchocutaneous fistula that can be detected by air leak guidance with or without fluoroscopy. Malignant peri-
in the water-seal chamber of the Pleur-evac. A large air cardial effusions have a high recurrence rate. Septic peri-
leak from a bronchocutaneous fistula can cause respira- cardial effusions are rare and are successfully drained
tory insufficiency in a critically ill patient. To avoid this percutaneously.
problem, the catheter used to drain a lung abscess should
be no larger than 12 to 14 Fr.
Liver (Online Case 75)
Mediastinal abscess is an emergent, life-threatening
infection that usually occurs after thoracic surgery or Pyogenic (bacterial) liver abscess may result from cholangi-
endoscopy.32 CT or sonography combined with fluoros- tis, iatrogenic or criminal trauma, hematogenous septic
copy is used for image-guided tube placement with a emboli from enteric abscesses (e.g., appendicitis, diver-
parasternal or paraspinous approach to avoid the lung ticulitis), or tumor.34 Percutaneous drainage has largely
(Fig. 5-10). replaced operative treatment.35 Acute cholangitis typi-
Pericardial effusions require drainage when there is im- cally develops in patients with partial or total biliary
pairment of diastolic filling of the ventricles. The causes obstruction caused by gallstones or tumor. PFD is well
of large symptomatic pericardial effusions include renal accepted as first-line therapy for these abscesses.36-38 Tube
insufficiency, metabolic or immunologic diseases, infec- insertion is done with sonographic or CT guidance. Care
tion, trauma (such as biopsy) and malignancy.33 Pericar- should be taken to avoid traversing the pleura, which
dial catheter drainage is performed under sonographic may lead to empyema. Percutaneous drainage can treat
C D
5. TRANSCATHETER FLUID DRAINAGE 117
the abscess and may decompress the biliary tree if there is Amebic abscess is diagnosed with serologic tests and is
distal biliary obstruction. However, additional biliary almost always eradicated with drug therapy such as met-
drainage may be required to control sepsis. PFD is not ronidazole. Indications for amebic abscess drainage
feasible for widespread microabscesses, but may still pro- include failure of medical therapy, perforated abscess,
vide benefit in complex or multiloculated collections.39 and large collections in a peripheral location or the left
Single-step needle aspiration without tube placement had lobe of the liver.50-52 Abscesses at these sites are prone
gained some popularity for noncholangitic pyogenic liver especially to rupture into the peritoneum, pericardium,
abscesses, but later studies questioned this approach.40-42 or pleural space. Percutaneous drainage effectively con-
Percutaneous needle aspiration without catheter place- trols symptoms from amebic abscess (Fig. 5-11). The
ment may have a role to play in the management of col- usual duration of catheterization is less than 1 week. An
lections that are too small to allow for catheter placement alternative approach is simple aspiration with a large-
(generally less than 5 cm in size), with catheter placement bore needle or single-step catheter drainage and removal.
showing greater benefit in larger lesions.43 Congenital liver cysts usually are multiple and fall
Hydatid cyst disease is caused by the parasite Echino- along the spectrum of polycystic kidney disease. Infre-
coccus granulosus. The characteristic CT finding is multi- quently, symptomatic dominant cysts require drainage
loculated hepatic cysts with daughter collections. Med- and sclerosis.53 However, solitary cystic liver lesions
ical therapy is the standard treatment.44 Invasive may be malignant (e.g., primary cystadenocarcinoma,
procedures (PFD or surgery) are reserved for failures of metastatic disease) and are treated by surgical resection.
drug therapy.45-47 In the past, PFD was avoided strictly Metastatic cystic tumors may benefit from palliative
because of the fear of leakage of scolices with ensuing drainage to alleviate mass effectcaused discomfort. The
anaphylactic shock or peritoneal spread. However, pub- method of cyst and lymphocele sclerotherapy are
lished series describe favorable results in controlling described later in this chapter.
the disease with a combination of oral albendazole and Post-traumatic biloma results from liver injury from
percutaneous drainage.48,49 Albendazole therapy begins blunt or penetrating trauma, or abdominal surgery.54,55
2 weeks before drainage and is continued until the cath- Bile accumulation from disrupted bile ducts may not
eter is removed. Puncture, aspiration, injection, and require drainage if it is small, sterile, and asymptomatic.
reaspiration (PAIR) technique is typically performed. Usually, though, bilomas become infected and require
To avoid seeding the abdominal cavity at the time of percutaneous drainage (Fig. 5-12). The presence of a
drainage, aliquots of hydatid-fluid aspirate should be biliary fistula may prolong the duration of catheteriza-
replaced with hypertonic (33%) saline solution. When tion. Biliary fistulas usually close unless there is total
the entire cyst is filled with saline solution, a catheter is transection of a bile duct or distal biliary obstruction.
inserted and left to gravity drainage. A catheter sino- Ischemic fluid collections are complex bilomas caused by
gram is performed later to assess communication with focal liver infarction. Liver infarcts result from severe
the bile ducts. If no communication is found, absolute compromise of the hepatic circulation and are seen in
alcohol is injected to assist in removal of the germinative patients with portal vein thrombosis, occlusion of
layer of the cyst. Bile staining or pus in the hydatid cyst branches of the hepatic artery, or profound hypotension.
cavity is a sign that the parasites are dead. Infarcts may become infected and require drainage.
A B
FIGURE 5-11 Amebic liver abscess drainage. A, Computed tomography scan shows two large, low-density masses with enhancing rims
and surrounding edema in the left lobe and caudate lobe. Numerous small satellite lesions were seen throughout the liver on other images.
B, A 22-gauge spinal needle was advanced into the left lobe cavity with sonographic guidance; frank pus was aspirated. A 12-Fr drainage
catheter was placed by tandem trocar technique. The caudate lobe lesion was drained in a similar fashion.
118 I. BASIC PRINCIPLES AND TECHNIQUES
A B C
D E F
FIGURE 5-12 Biloma drainage after iatrogenic trauma during laparoscopic cholecystectomy. A, Computed tomography (CT) scan shows
large, low-attenuation hepatic fluid collection consistent with biloma. B and C, Ultrasound demonstrates the mixed echogenicity collection and
needle access. D, Fluoroscopy after ultrasound-guided needle access demonstrates wire placement. E and F, The track is dilated, followed by
pigtail drainage catheter placement.
These collections are filled with necrotic liver paren- from adjacent tissue. Tube insertion is done with sono-
chyma and bile. A biliary fistula is the rule after percuta- graphic or CT guidance63 (see Fig. 5-1). Care should be
neous drainage. Catheter sinograms reveal necrotic ma- taken to avoid transgressing bowel, kidney, or pancreas.
terial in the bile ducts, which can cause biliary obstruction Transpleural drainage is not recommended but can
and maintain the fistula. Resolution of ischemic bilomas be done safely.64 To prevent splenic hemorrhage, the
depends on adequate drainage, unobstructed bile ducts, catheter is inserted by traversing the least amount of
and appropriate nutrition and vascular supply to allow splenic parenchyma possible.
for liver regeneration and healing of the collection cavity.
Pancreas
Spleen Basic management of all pancreatic fluid collections in-
Percutaneous drainage of splenic fluid collections is cludes bowel rest, parenteral antibiotics, and parenteral
done for abscesses, liquefied infarcts, and symptomatic or enteral nutrition. PFD is indicated for pancreatic pseu-
cysts.56-59 Although splenic fluid collections are relatively docysts that become infected or cause symptoms such
rare, these can be safely approached by percutaneous as continued pain or bowel or biliary obstruction65,66
means.60,61 Drainage may be performed as a temporizing (Fig. 5-13). Percutaneous drainage also plays a major
measure before splenectomy, or even as a curative mea- role in the management of necrotic collections and pan-
sure with antibiotic therapy and without need for subse- creatic abscesses67-69 (Fig. 5-14).
quent surgery.62 Abscesses and pseudocysts may spread to the lesser
Splenic abscesses are caused by hematogenous seeding sac, paracolic gutter or pararenal space, pelvis, and
(as in intravenous drug abusers) or trauma or are spread occasionally the thorax. Pancreatic phlegmon does not
5. TRANSCATHETER FLUID DRAINAGE 119
C D
C D
120 I. BASIC PRINCIPLES AND TECHNIQUES
A B
The transrectal approach is useful for infected collections Patients tolerate transvaginal and transrectal catheters
adjacent to the rectum.89-91 Sterile collections may become surprisingly well.
infected if drained in this fashion. Access is gained using
an endocavitary sonographic probe (with biopsy guide) Sclerotherapy of Lymphoceles and Cysts
and fluoroscopy or CT guidance with the patient in a
(Online Case 15)
lateral decubitus position (Fig. 5-16). A Foley catheter is
inserted into the bladder prior to transrectal and trans- Lymphoceles usually are secondary to pelvic operations,
vaginal drainage to allow better visualization of the particularly kidney transplantation and lymph node dis-
collection and to minimize the risk of bladder puncture. section. PFD is the procedure of choice but may require
The transvaginal approach is exceedingly useful in protracted tube placement ("1 month).
women with fluid collections in contact with the vaginal Management of true cysts and lymphoceles often
wall.92,93 It is performed with a vaginal sonographic requires intracavitary injection of a sclerosing agent.94-96
probe (with a biopsy guide) and fluoroscopic guidance Before sclerosis is performed, a catheter sinogram is per-
(Fig. 5-17). Catheter insertion through the muscular formed to exclude communication of the drained cavity
vaginal wall may be difficult. with vital structures such as vessels, ductal structures, or
Catheters placed transvaginally or transrectally ben- bowel. The amount of contrast injected for the sinogram
efit from having a locking pigtail loop (Cope) to prevent allows for a measurement of the volume of sclerosant to be
dislodgment when the patient is upright. The catheter is used. Sclerosis is successfully achieved by multiple injec-
secured to the skin of the medial aspect of the thigh. tions of absolute alcohol, tetracycline, or iodine solutions.
122 I. BASIC PRINCIPLES AND TECHNIQUES
C D
Barring the discovery of a fistula during sinography, managed successfully with PFD (see Chapter 23).
the cavity is injected with the sclerosing agent until there Urinoma drainage usually is done after percutaneous
is complete filling of the space without excessive pres- nephrostomy to divert the urine flow that maintains the
sure. The catheter is then clamped. The patient is al- collection. Renal abscesses usually have a phlegmonous
lowed to move about for approximately one hour, with component that may not respond to percutaneous drain-
a variety of maneuvers employed to ensure contact of age. Symptomatic simple renal cysts are treated with
the sclerosing agent with all walls of the cavity. The cath- catheter drainage and sclerosis.
eter is then reopened to gravity drainage. Patients are
instructed to record drainage output daily, with the
Musculoskeletal System
expectation that output should diminish after each
sclerotherapy procedure. The procedure is repeated Muscular abscesses, hematomas, and lymphoceles are
within one week, again starting with a sinogram to successfully drained percutaneously. Abscess recur-
document the size of the cavity prior to sclerosis. The rence caused by osteomyelitis depends on control of
catheter is removed when output has decreased to less the bone infection. Hip effusions also have been
than 10 mL/day and sinography demonstrates near drained percutaneously. Few data are available on
complete collapse of the cavity. the success rate of percutaneous drainage for joint
effusions.
Iliopsoas muscle abscesses usually originate from an
Kidney and Retroperitoneum (Online Case 35) axial skeletal infection or other adjacent process (e.g.,
Retroperitoneal collections include urinomas, perineph- diverticulitis, appendicitis, infected lymph nodes).98
ric abscess, renal abscess, renal cysts, iliopsoas muscle Bilateral iliopsoas abscesses are usually caused by spon-
abscess, and necrotic tumors (most commonly cervical dylitis. The offending organism is often Mycobacterium
carcinoma metastases).97 Most of these collections can be tuberculosis (Fig. 5-18).
5. TRANSCATHETER FLUID DRAINAGE 123
A B C
D E F
FIGURE 5-17 Transvaginal drainage of pyometrium caused by cervical obstruction from carcinoma. A, The uterus is dilated and fluid
filled. B, Sagittal transvaginal sonography identifies the dilated uterus (u), cervix (c), and bladder with indwelling Foley catheter (b). C, The
transvaginal needle is advanced into the uterus. D, A guidewire is inserted through the needle. E, A 10-Fr drainage catheter is advanced over
the guidewire. F, Final catheter placement in the uterine cavity.
C D
124 I. BASIC PRINCIPLES AND TECHNIQUES
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22. Kraus GJ. The split pleura sign. Radiology 2007;243:297. Am J Roentgenol 1995;165:1163.
23. Lee MJ, Saini S, Brink JA, et al. Interventional radiology of the 46. Bret PM, Fond A, Bretagnolle M, et al. Percutaneous aspiration and
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24. Merriam MA, Cronin JJ, Dorfman GS, et al. Radiographically cyst: successful percutaneous drainage. Radiology 1985;155:627.
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1995;20:65. endoscopy-assisted removal of necrotic debris from pancreatic fluid
51. vanSonnenberg E, Mueller PR, Schiffman HR, et al. Intrahepatic collections. Baltimore (MD): SCVIR 27th Annual Scientific Meeting,
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52. Ken JG, vanSonnenberg E, Casola G, et al. Perforated amebic liver copy and endoscopic retrograde cholangiopancreatography in
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53. vanSonnenberg E, Wroblicka JT, DAgostino HB, et al. Symptom- 2005;19:393.
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57. Ng KK, Lee TY, Wan YL, et al. Splenic abscess: diagnosis and man- tory masses: CT directed management and clinical outcome in
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58. Thanos L, Dailiana T, Papaioannou G, et al. Percutaneous CT- 82. Neff CC, vanSonnenberg E, Casola G, et al. Diverticular abscesses:
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59. Tasar M, Ugurel MS, Kocaoglu M, et al. Computed tomography- 83. Mueller PR, Saini S, Wittenberg J, et al. Sigmoid diverticular ab-
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60. Kang M, Kalra N, Gulati M, et al. Image guided percutaneous 84. Ambrosetti P, Chautems R, Soravia C, et al. Long-term outcome of
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72. Fotoohi M, DAgostino HB, Wollman B, et al. Persistent pancreato- erative lymphoceles with percutaneous drainage and alcohol
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S E C T I O N II
6
Thoracic Aorta
Karim Valji
ARTERIOGRAPHY connect these two major vascular channels (Fig. 6-1 and
Table 6-1). The normal left aortic arch persists while the
Thoracic aortography usually is done through a femo- right arch involutes beyond the origin of the right subcla-
ral artery approach. In individuals with a history of vian artery. The remaining portion of the right arch
catheterization-related cholesterol embolization, angi- becomes the brachiocephalic (innominate) artery.
ography is sometimes performed via the proximal left
brachial artery to avoid recurrent showering of plaque
Normal Anatomy
fragments. Although catheter angiography is rarely
required in patients with suspected traumatic aortic The aortic valve is composed of three leaflets that form
injury, in that situation the arch should be traversed the three sinuses of Valsalva: right, left, and posterior or
with a guidewire. Advancing a formed pigtail catheter noncoronary3 (Fig. 6-2). The right and left coronary arteries
into a traumatic pseudoaneurysm can be lethal.1 arise from their respective sinuses. Beyond the sinus
A pigtail or similarly shaped catheter is placed about segment, the ascending aorta courses anteriorly and
2 cm above the aortic valve to avoid catheter recoil superiorly. This region is enclosed within the fibrous
into the left ventricle during rapid contrast injection. pericardium. In adults, its mean diameter at end diastole
A steep right posterior oblique projection is standard. is 2.8 cm.4 The aorta then passes over the main pulmonary
Additional projections are obtained as needed. artery and left main stem bronchus. The brachiocephalic,
left common carotid, and left subclavian arteries take off in
turn from the upper surface of the aortic arch.
ANATOMY Just beyond the origin of the left subclavian artery, the
aorta narrows at the aortic isthmus. It then widens slightly
beyond this point at the aortic spindle. The ligamentum arte-
Development riosum, a remnant of the ductus arteriosus, tethers the
In the fetus, two paired blood vessels (dorsal and ventral aorta to the left pulmonary artery at the isthmus. In some
aortae) form in the chest.2 The ventral aortae merge into the cases, a shallow, smooth, symmetric outpouching persists:
aortic sac, which forms parts of the ascending aorta, aortic the ductus diverticulum, or ductus bump (Fig. 6-3).
arch, and pulmonary trunk. The left dorsal aorta becomes The descending thoracic aorta runs in front of the
the descending thoracic aorta. Six pairs of branchial arches spine. In adults, its mean diameter at end diastole is
ICA ECA
129
130 II. AORTA AND PERIPHERAL ARTERIES
Right
subclavian
artery
Left
subclavian FIGURE 6-3 Normal thoracic aortogram in left posterior oblique
artery projection demonstrates a prominent ductus diverticulum (arrow).
artery from the root of the brachiocephalic artery (bovine in cattle. Takeoff of the left vertebral artery directly from
arch) is reported in 3% to 29% of the population based on the arch is an uncommon variant (see Fig. 6-4). Separate
autopsy and imaging studies; the true figure is probably origin of the right subclavian and common carotid arter-
closer to 10% to 15%7,8 (Fig. 6-4). The origin of the term ies from the arch is rare.
bovine arch is disputed. It may reflect the configuration of An aberrant right subclavian artery is the most common
the vessels (like a bulls horn); this anatomy is not typical aortic arch malformation of clinical significance, with a
reported frequency of 0.4% to 2.3%.9 This anomaly
results from involution of the embryonic aortic segment
between the right subclavian and right common carotid
arteries. The right subclavian artery becomes the last
branch of the aortic arch (Fig. 6-5). It usually passes
behind the trachea and esophagus to reach the right side
of the chest. The vessel may indent the posterior surface
of the esophagus, but patients rarely have symptoms.10
The aberrant artery often originates from a dilated
portion of the most distal remnant of the right aortic
arch, the so-called diverticulum of Kommerell.
Right aortic arch with aberrant left subclavian artery is the
most common of the several types of right aortic arch,
occurring in about 0.1% of the population.11 The root
cause is involution of the left aortic arch between the left
common and left subclavian arteries with persistence of
the embryologic right arch. The order of aortic arch
branching is therefore left carotid artery, right carotid
artery, right subclavian artery, and left subclavian artery.
The arch passes over the right main stem bronchus and
descends on either side of the spine (Fig. 6-6). Despite
the presence of a vascular ring, respiratory and esopha-
geal symptoms are infrequent. Few of these individuals
have associated congenital heart disease.
Right aortic arch with mirror-image branching imposes a
branch order of left brachiocephalic artery, right common
FIGURE 6-4 Bovine aortic arch (large arrow) with anomalous carotid artery, and right subclavian artery.12 The descend-
origin of left vertebral artery from the aortic arch (small arrow). ing thoracic aorta is virtually always to the right of the
A B
FIGURE 6-5 Aberrant right subclavian artery. A, The artery runs posterior to the trachea and esophagus on computed tomography
angiography. B, Aberrant vessel arises as the last branch of the aortic arch on black-blood magnetic resonance image. (Courtesy of Eric
Goodman, MD, San Diego.)
132 II. AORTA AND PERIPHERAL ARTERIES
B C
FIGURE 6-6 Right aortic arch with aberrant left subclavian artery. A, Chest radiograph shows right-sided aorta displacing the trachea to
the left. B, Coronal three-dimensional MR angiography with cine breath-hold technique shows the right aortic arch. C, The left subclavian artery
is the final branch of the aortic arch and arises from a large diverticulum.
spine. Some form of congenital heart disease is found in peripheral circulation. Emboli usually are released from
90% to 95% of patients, including tetralogy of Fallot, trun- protruding plaques with a mobile component that is
cus arteriosus, double-outlet right ventricle, and transpo- probably overlying thrombus.13 Most of these symptom-
sition of the great vessels. About one third of patients with atic lesions are found in the aortic arch and descending
tetralogy of Fallot have a right aortic arch, usually of this thoracic aorta. About one third of patients with such
type. Although the vascular ring created by the right arch atheromas suffer distal embolization within 1 year of
and ligamentum arteriosum produces tracheal or esopha- detection. Cholesterol crystals may shower into the dis-
geal compression, patients usually have no symptoms. tal circulation (spontaneously or after aortic manipula-
tion) and result in renal insufficiency, bowel ischemia, or
blue toe syndrome.14
MAJOR DISORDERS Suspected thoracic aortic atherosclerosis in patients
with unexplained stroke or peripheral embolization is
studied by transesophageal echocardiography (TEE),
Atherosclerosis
computed tomography (CT), magnetic resonance im-
Atherosclerosis is the most common disease affecting aging (MRI), or positron emission tomography (PET)
the thoracic aorta, but usually it is silent. Plaques cause imaging.13,15 The disease produces an irregular contour
symptoms when fragments embolize into the brain or to the aortic lumen, typically in the arch or distal aorta
6. THORACIC AORTA 133
BOX 6-2
C AU S E S O F T H O R A C I C
A O RT I C A N E U RY S M S
Degenerative (atherosclerotic)
Bicuspid aortic valve
Trauma
Blunt or penetrating
Postoperative
Chronic dissection
Noninflammatory vasculopathy
Marfan syndrome
Ehlers-Danlos syndromes
Loeys-Dietz syndrome
Infection (bacterial, syphilitic, tuberculous)
Vasculitis (see Box 6-5)
Congenital (sinus of Valsalva aneurysm)
reasons. Unusual complaints related to compression of An interposition graft is placed by end-to-end anasto-
adjacent organs include dysphagia, respiratory dis- mosis of a synthetic conduit between the excised ends of
tress, superior vena cava syndrome, and hoarseness the aorta. Alternatively, the diseased portion of the aorta
from impingement of the recurrent laryngeal nerve. is wrapped around the graft material sewn to the aorta
Some individuals with intact aneurysms do complain at both ends as an inclusion graft. With proximal aortic
of chest or back pain. However, symptoms are ex- disease, an elephant trunk technique may be employed.31
pected when the aneurysm ruptures. They include The ascending aortic and arch segments are replaced
chest pain, hypotension, massive hemoptysis (from with graft material and branch vessels connected into it;
aortobronchial fistula), hematemesis (from the even rarer the distal free end of the graft floats in the descending
aortoesophageal fistula), and dyspnea from leakage into thoracic aorta. At a later stage, the surgeon creates a
the pleural space. permanent anastomosis to the normal lower descending
thoracic aorta.
Major complications of operative TAA repair include
Imaging
stroke, myocardial infarction, and renal failure. Paraple-
CHEST RADIOGRAPHY gia is a rather unique and devastating event caused
Plain chest radiographs show enlargement of the as- by exclusion of branches to the spinal artery. It is more
cending aorta, descending aorta, or both. A massive frequent with repair of thoracoabdominal aneurysms.
aneurysm can erode the vertebral bodies or sternum. The frequency of spinal cord injury is well under 10%
Atelectasis can result from compression of the airways. with the use of intraoperative maneuvers such as distal
A left pleural effusion suggests the possibility of rupture. perfusion, hypothermia, and monitoring of evoked
potentials.32,33 Preoperative spinal arteriography may be
TRANSESOPHAGEAL ECHOCARDIOGRAPHY useful in this setting to allow reimplantation of major
TEE can both detect and size TAA.26 However, TEE is spinal artery branches.34 In contemporary series, the
less valuable for aneurysm staging, evaluation of adja- overall mortality rate for elective repair is still substan-
cent structures, or postoperative surveillance. tial but far better than for operation with rupture (3% to
8% vs. 22%).32,33
COMPUTED TOMOGRAPHY
CT is the standard tool for the diagnosis of suspected ENDOVASCULAR THERAPY
TAA, surveillance of known aneurysms, and detection Thoracic endovascular aneurysm repair (TEVAR) with
of sac rupture.27 Aneurysm diameter and length, presence stent grafts is an attractive alternative to open surgery
of mural thrombus, and associated atherosclerotic dis- for selected patients with stable or ruptured degenera-
ease are well depicted by CT (Fig. 6-8). A high-density tive TAAs.35-37 Several devices are approved by the U.S.
crescent in the mural thrombus may be a harbinger of Food and Drug Administration for treatment of this
contained or imminent rupture. Multiplanar reformatted particular disorder (Table 6-3 and Fig. 6-9). The choice
and shaded-surface display images provide exquisite of stent graft is based on patient factors, aneurysm char-
views of the aneurysm, its relationship to adjacent struc- acteristics, and operator preference. The TAG device can
tures (e.g., compression of the pulmonary artery), and be inserted rapidly but with somewhat less precision
involvement of arch vessels.16,28 than other endografts. The Talent device (and the newer
iteration Valiant stent) allows accurate deployment and
MAGNETIC RESONANCE IMAGING is easier to use with severe aortic angulation or iliac
MRI is probably the best modality for studying TAA in artery access tortuosity. Finally, the Zenith device has the
patients in stable condition, although it is not effective lowest profile (at present) and permits the most accu-
after endograft repair. Gadolinium-enhanced MR angi- rate deployment.
ography characterizes the entire extent of the aneurysm, Technical success and immediate aneurysm throm-
its effect on neighboring organs, branch vessel involve- bosis is noted in more than 90% of cases with very low
ment, the aortic valve, and the heart.6,29 Several features mortality rates38 (see Fig. 6-8). Unlike endograft treat-
can sometimes differentiate degenerative aneurysms ment of abdominal aortic aneurysms (see Chapter 7),
from other types (see Table 6-2). the most common type of endoleak with TAA (up to
30% of cases) is a type I defect at an attachment
site.39,40 In this situation, additional interventions
Treatment
(further balloon treatment, insertion of additional
SURGICAL THERAPY stents or stent grafts) are usually necessary. Uncom-
The traditional treatment for TAAs is operative.30 As a mon early complications include stroke and para-
rule, they are repaired when the diameter exceeds 5 to plegia from exclusion of side branches feeding the
6 cm or the patient is symptomatic (see earlier discussion). spinal cord.41 Late complications involve proximal
6. THORACIC AORTA 135
A B C
D E F
FIGURE 6-8 Stent graft repair of a degenerative thoracic aortic aneurysm. A and B, On contrast-enhanced computed tomography
(CT) scans, two regions of saccular dilation of the descending thoracic aorta (almost extending to the abdominal segment) are evident.
C, The stent graft is in place and is widely patent. D, On follow-up CT, a crescentic region of contrast appears outside the graft but within
the aneurysm sac (arrow). E and F, Catheter aortography demonstrates the leak that occurs at a graft attachment site (arrow).
and distal endoleaks, aneurysm growth at the edges better 1-year mortality with TEVAR, whereas the other
of the device, stent graft movement, kinking or frac- showed no difference at 2 years. A recent metaanalysis
ture, and aneurysm rupture. calculated a significantly lower incidence of neurologic
The choice between open and endovascular repair injury and perioperative mortality with TEVAR.
of TAA is made difficult by the almost complete lack
of randomized, controlled trials comparing the two ap- Dissection (Online Cases 13 and 52)
proaches.36,37 Two large, prospective, single-arm trials with
historical controls noted significantly lower early mor- Etiology
bidity and mortality and paraplegia rates with TEVAR.38,42 A dissection is a longitudinal split in the media of
Reported outcomes were technical success 96%, major the aortic wall. In most cases, an intimal tear connects
adverse events 41%, 30-day mortality 2.1%, paraplegia this medial channel with the aortic lumen. Dissections
1.5%, stroke 3.6%, aneurysm rupture at 1 year 0.5%, confined to the aortic wall are intramural hematomas43
migration 4%, and endoleak 12.2%. One study observed (see later discussion).
136 II. AORTA AND PERIPHERAL ARTERIES
TABLE 6-3 FDA-Approved Stent Grafts for use (particularly cocaine and methamphetamines) is
Thoracic Aortic Disease being recognized as an increasingly frequent cause
Type Talent Zenith TAG
of acute dissection.46 Occasionally, aortic dissection is
caused by trauma (e.g., deceleration injury, catheter-
Manufacturer Medtronic Cook, Inc W.L. Gore ization procedures).47
Associates
Regardless of the underlying pathology, the inciting
Components Single Two part Single
Construction Nitinol/ Stainless steel/ Nitinol/ePTFE event usually is an intimal tear. Sometimes, the dissec-
polyester Dacron tion begins spontaneously within the aortic wall, pos-
Bare segment Available Available sibly from rupture of the vasa vasorum. The intimal
Delivery system 22-25 Fr 20-22 Fr Large tear connects the lumen in direct continuity with the
Device diameter 22-46 mm 22-42 mm 26-40 mm
aortic valve (true lumen) with the channel of blood in
Device length 10.8-21.6 cm 10, 15, 20 cm
Features Very flexible Low profile Easy deployment the media (false lumen). The dissection propagates dis-
Very trackable Precise tally, proximally, or in both directions as blood
Wide size placement under high pressure expands the false channel. Blood
range flow in the false lumen usually is slower than in the
ePTFE, expanded polytetrafluoroethylene. true lumen. The false channel, however, can become
large and compress the true lumen. The dissection
usually stops at an aortic branch or atherosclerotic
The pathogenesis of aortic dissection is not entirely plaque. In many cases, it extends to the aortic bifurca-
understood.44 Dissection is usually attributed to tion or beyond.
hemodynamic stresses such as long-standing hyper- The location and extent of the dissection has impor-
tension or to abnormalities of the media (some of tant implications for treatment and prognosis. The
which are congenital)45 (Box 6-3). In the former group, DeBakey and Stanford classifications are illustrated in
the pathologic basis for dissection is unclear; only Figure 6-10. Stanford type A dissections, which usually
mild medial degeneration is seen histologically. In the begin with a tear just above the aortic valve and always
latter group, degeneration of medial smooth muscle, involve the ascending aorta, account for about two
elastin, or collagen matrix can be identified. The thirds of cases.48 Type B dissections, which usually begin
reason that pregnant women are at greater risk for dis- with a tear just beyond the origin of the left subclavian
section is unknown, although hemodynamic factors artery and only involve the descending aorta, account
and hormonal effects have been implicated. Illicit drug for the remaining cases. Sometimes, a dissection that
A B C
FIGURE 6-9 Stent graft devices for thoracic aortic disease. A, TAG graft. B, Zenith graft. C, Schematic of Zenith graft for exclusion of a
descending thoracic aortic aneurysm. (A, Courtesy of W.L. Gore Associates; B, Courtesy of Cook, Inc.)
6. THORACIC AORTA 137
A B
C D
FIGURE 6-11 Stanford type A aortic dissection. A and B, Contrast-enhanced chest computed tomography shows a complex dissection
flap passing through the entire aortic arch. Spot of calcification on lateral wall of arch denotes the intima (arrow), indicating that the true
lumen is lateral and false lumen more medial at that level. C, The compressed true lumen (arrow) supplies the superior mesenteric artery.
D, The true lumen also supplies the left renal artery (arrowhead).
Other possible findings are dilation of the aorta, compres- scanning times and difficulties with monitoring critically
sion of the true lumen by the false lumen, thrombosis ill patients. Cine imaging will help detect aortic insuffi-
of the false lumen, mediastinal hematoma, and pleural ciency. MR images can identify an intimal flap and differ-
or pericardial effusion. A localized dissection must be dif- ent signal intensities in the true and false lumens caused
ferentiated from an intramural hematoma or a penetrating by variations in blood flow or by clot (Fig. 6-13). Noncom-
aortic ulcer (see later discussion). municating dissection (i.e., intramural hematoma) can
It is important to distinguish the true lumen from usually be differentiated from a communicating dissection
the false lumen and the relationship of all major aortic with slow flow.
branches to them. The true lumen is the one in continu-
ity with the aortic valve. The most reliable features of TRANSESOPHAGEAL ECHOCARDIOGRAPHY
the true lumen are outer wall calcification and eccentric TEE is performed with multiplanar color flow Doppler
flap calcification53 (see Fig. 6-11). The false lumen usu- techniques.26 The procedure can be performed at the
ally has a larger cross-sectional area and an acute angle bedside in less than 30 minutes with the patient under
between the flap and the outer aortic wall (Fig. 6-12). In moderate sedation. TEE is favored by cardiologists
most type B aortic dissections, the false lumen is poste- because it is fast and convenient. Besides identifying
rior and lateral to the true lumen in the chest and then an intimal flap, echocardiography also can detect aortic
spirals down the aorta in a somewhat unpredictable insufficiency and extension of dissection into the coro-
fashion. nary arteries. It is extremely sensitive but somewhat less
specific than CT and MRI. The aortic arch is a relative
MAGNETIC RESONANCE IMAGING blind-spot for this modality.
Gadolinium-enhanced MR angiography also is extremely
accurate for diagnosing and staging aortic dissection.29,54,55 CATHETER ANGIOGRAPHY
The risks of iodinated contrast material are avoided. Aor- Aortography was once the primary method for preoper-
tic branch vessels, the aortic valve, and the heart can ative diagnosis of aortic dissection but is now only neces-
be evaluated with MRI. Its major limitations are longer sary prior to TEVAR or other endovascular interventions.
6. THORACIC AORTA 139
T
F
A B C
D E F
FIGURE 6-12 Stanford type B dissection (A and B) with extension into the abdominal aorta seen with computed tomography angiography
(T, true lumen; F, false lumen). Note relationship of lumens to celiac (C), superior mesenteric (D), right renal (E), and left renal arteries into
which the dissection flap extends (F). The dissection continued down both iliac arteries to the groin (not shown).
Treatment
Aortography is more risky and less sensitive than cross-
sectional techniques in the detection of acute dissection. SURGICAL THERAPY
The imager can entirely miss the diagnosis of intramural Management of patients with acute aortic dissection
hematoma or chronic dissection with thrombosis of the depends on the location and extent of the dissection,
false lumen. existence of complications, and the general health of the
CT or MR images guide catheterization of the true patient. Patients with type B dissection are first treated
and/or false lumens from a common femoral or brachial medically with blood pressure control. There is a con-
artery approach. Special care should be taken to avoid sensus that most patients with Stanford type A dissec-
extending or overinjecting the false lumen if it is cathe- tion should undergo repair with graft insertion or pri-
terized. Abdominal or pelvic arteriography usually mary obliteration of the false lumen.44,50 The aortic valve
is needed to follow the dissection to the level of reentry. is replaced when necessary. Repair is performed if there
A lucent flap between the true and false lumens is diag- is a complication (e.g., renal failure, mesenteric isch-
nostic (Fig. 6-14). Delayed filling and slow washout of emia), rapid expansion, or impending rupture signaled
the false lumen are characteristic. The true lumen may by continuing pain or hypotension. Notably, mortality
be narrowed by an expanding false channel. The rela- rates are substantially reduced if mesenteric ischemia
tionship of branch vessels to the two lumens should be (when present) is treated before attending to the aortic
established. pathology itself.57 Chronic dissections usually are treated
when the aortic diameter exceeds 6 cm or the patient has
CHOICE OF IMAGING MODALITY symptoms.
Multidetector CT and MR angiography have similar
accuracy in the diagnosis of aortic dissection.29,56 The ENDOVASCULAR THERAPY
optimal approach to the patient with suspected or Endovascular methods have been devised to treat both
known dissection depends on the relative availability acute and late complications of aortic dissection. These
of equipment, condition of the patient, and capability of techniques include uncovered stent placement, balloon
operators. fenestration, and stent graft insertion.
140 II. AORTA AND PERIPHERAL ARTERIES
C D
Clinical Features
The violence of the event may not correlate with the like-
lihood of aortic injury. Clinical symptoms and signs are
not particularly helpful in screening patients. For these
reasons, every patient with the appropriate mechanism
of injury is suspect. Because the consequence of missing
an aortic injury is so grave, imaging studies are used
liberally.
Imaging
CHEST RADIOGRAPHY
A plain radiograph is obtained for every patient with
significant chest trauma. Radiographs are most useful
with the patient in an upright position, although this is
rarely feasible. A ruptured aorta produces a host of find-
ings69 (Box 6-4). The most sensitive signs are widening of
the superior mediastinum (ultimately a subjective call),
FIGURE 6-16 The supine chest radiograph of a patient with a
indistinctness of the aortic arch contour, and loss of the
traumatic aortic tear shows marked widening of the mediastinum
descending aortic shadow (Fig. 6-16). Fewer than 1% to and loss of the normal aortic knob.
2% of patients with normal chest radiographs are subse-
quently found to have an aortic laceration. In practice,
most stable patients with a mechanism for injury pro- must be taken to identify abnormalities at the origins of
ceed to CT scanning. the arch vessels.
A B
FIGURE 6-20 A, Standard right posterior oblique projection shows no evidence of blunt aortic injury. B, Shallow left posterior oblique
projection shows abnormal outpouching from the proximal descending thoracic aorta (arrow).
FIGURE 6-21 Traumatic rupture at the aortic isthmus on right FIGURE 6-22 Subtle intimal flap in the upper descending thoracic
posterior oblique arch aortography. aorta (arrow) from a deceleration injury (confirmed at operation).
6. THORACIC AORTA 145
A B
FIGURE 6-23 A, Bronchial artery diverticulum (arrow) and aberrant right subclavian artery on arch aortography. B, In steep right posterior
oblique projection, a diverticulum of Kommerell (K) is evident.
OTHER MODALITIES
In general, TEE and MRI are not favored for the evalua- an American Society for the Surgery of Trauma multi-
tion of blunt aortic trauma except to confirm other center prospective nonrandomized trial.47 About two
equivocal studies.75 IVUS detects many of the typical thirds of 193 patients underwent endograft insertion,
findings of acute aortic injury.76,77 Although its accuracy and the remainder were treated with open operation.
is debated, it can be a valuable adjunct during endograft Mortality and paraplegia rates were significantly
placement. lower in the endograft group (7.2% vs. 23.5% and 0.8%
vs. 2.9%, respectively). There were comparable rates
of adverse events in the two cohorts. Endoleak was
Treatment
detected in 14.4% of the former group; most required
SURGICAL THERAPY additional device placement or conversion to open
Traditionally, all acute traumatic aortic injuries were surgery. Notably, the mean interval between injury
repaired immediately with primary resection or graft and definitive treatment was slightly more than
placement.78 Recent trends in trauma care favor a slight 2 days. These conclusions are further supported by a
delay in repair (open or endovascular), particularly in recent meta-analysis of the published reports on the
patients with severe intracranial injury or at high risk subject.79
for thoracic surgery.47,79,80 Beta-blocking agents are used Criteria for selection of patients is both device-
liberally to lower blood pressure and heart rate and thus and operator-dependent. The most important factors
avoid free rupture before definitive treatment. Small are:
intimal flaps may be managed medically with vigorous
imaging follow-up. Chronic pseudoaneurysms usually Length of the proximal landing zone (10 to 15 mm)
require surgical treatment. beyond the left subclavian artery (or left common
carotid artery if necessary)
ENDOVASCULAR THERAPY Aortic diameter (measured at several sites 1 to
Recently, endovascular stent grafts have become the 2 cm from landing zones) compatible with current
first line treatment for blunt aortic injury at many devices
major trauma centers79,81 (Fig. 6-24). To date, no ran- Femoral/iliac access artery that will accommodate
domized trials have compared stent graft and open device sheaths (typically 6 to 7 mm)
treatment. The most convincing evidence comes from Aortic arch angulation
146 II. AORTA AND PERIPHERAL ARTERIES
A B
C D
FIGURE 6-24 Traumatic aortic injury. A and B, Axial contrast-enhanced computed tomography scans of the chest show a focal, irregular
outpouching of the proximal descending thoracic aorta (arrow). Fluid density is present around the aorta at this level. A left chest tube is in
place. There is bilateral lung consolidation. C and D, A stent graft is placed to repair the injury and avoid surgery.
OTHER DISORDERS
A B
FIGURE 6-25 Takayasu arteritis. A, Gadolinium-enhanced magnetic resonance angiogram shows aortic wall thickening and enhancement.
B, Maximum intensity projection image shows long, smooth left common carotid artery (CCA) and left subclavian and right subclavian
artery stenoses with dilation of the upper left CCA.
thrombi, and, rarely, aortic insufficiency or dissection in the sinotubular portion of the ascending aorta and
(Fig. 6-25). may extend into the ventricular septum and mitral valve
In the quiescent phase of TA, branch obstructions apparatus. Aortic regurgitation can result; dilation of the
are treated if there is end-organ ischemia (e.g., arm aortic root is unusual.
claudication). Balloon angioplasty is an attractive
alternative to open surgery. Angioplasty is initially
Noninflammatory Vasculopathies
effective and safe for descending thoracic, abdominal
aortic, and pulmonary artery stenoses. Early series
(Online Case 62)
suggested that restenosis was uncommon.89-91 How- Marfan syndrome is an autosomal dominant disorder that
ever, one recent series found an unacceptably high affects the eyes, skeleton, muscles, and cardiovascular
rate of late failure of angioplasty alone in a cohort system98 (see Chapter 1). The disease mutation in the
of U.S. patients with symptomatic TA.92 Intravascular FBN1 gene that codes for fibrillin-1 results in structur-
stents have been used as an adjunct to angioplasty, ally deficient microfibrils in the aortic media and activa-
but should only be employed when absolutely tion of media-destroying matrix metalloproteinases by
necessary.93 It is advisable to delay surgery or percu- upregulated transforming growth factorbeta (TGF-#)
taneous therapy until the acute constitutional symp- levels.20,99 The cellular structure of the media becomes
toms have subsided.94 Expanding aneurysms often disorganized and weakened. However, up to one third
require operative repair, although stent grafts have of patients have a de novo noninherited defect. Affected
been used in this setting.95 individuals have characteristic thinning and elongation
Giant cell (temporal) arteritis is a vasculitis of large- and of the limbs along with other outward features. Cardio-
medium-sized arteries.82,83,96 The disease has some vascular complications are frequent and include aneu-
features in common with Takayasu arteritis but is a dis- rysm or dissection of the proximal ascending aorta,
tinct entity (see Chapter 1). Significant aortic disease, aortic insufficiency, mitral valve prolapse or calcifica-
such as aneurysm, annular dilation, or aortic insuffi- tion, and pulmonary artery dilation.100 Aortic dilation in
ciency, is relatively uncommon. Involved aortic branches Marfan syndrome usually is confined to the aortic root,
have long, smooth stenoses alternating with normal producing sinotubular ectasia with a characteristic tulip
segments. These findings, along with the distribution of bulb appearance101 (Fig. 6-26). The risk for type A dis-
disease, sometimes distinguish giant cell arteritis from section increases substantially when the aortic diameter
atherosclerosis. exceeds 5 cm, growth rate accelerates ($0.5 cm/year), a
Collagen-vascular disorders, particularly those linked to family member suffered dissection, or a woman be-
the HLA-B27 antigen, occasionally produce aortitis.97 comes pregnant.98 In such cases, operative aortic re-
Acute inflammation followed by fibrotic scarring occurs placement is indicated.
148 II. AORTA AND PERIPHERAL ARTERIES
A B
Ehlers-Danlos syndromes are a set of distinct genetic penetrating trauma. The inflamed wall can form an
disorders of collagen production102 (see Chapter 1). The infected (mycotic) aneurysm or pseudoaneurysm.109
rare vascular subtype (type IV) results from a genetic Although infectious aneurysms are rare, the aorta and
defect in type III procollagen. Translucent skin, easy femoral artery are the most commonly affected sites.
bruising, and pneumothorax are present. The vascular The usual pathogens are Salmonella species and Staphy-
manifestations are spontaneous arterial ruptures, aneu- lococcus aureus.110
rysms, occlusions, and arteriovenous or carotid-cavern- Some patients have localized pain, fever, and posi-
ous fistula. Historically, angiographers were warned to tive blood cultures. With this clinical picture, the
avoid catheterization in this population because of fears presence of an uncalcified, smooth, eccentric saccular
of severe complications.103 In fact, arteriography and aneurysm is highly worrisome for mycotic aneurysm
endovascular treatment can be done safely in many (Fig. 6-28). Tuberculous aortitis may develop from lym-
patients.104 phangitic spread or contiguous extension of disease in
Loeys-Dietz syndrome is a recently identified autoso- the chest. Syphilitic aortitis has been largely eradicated
mal dominant connective tissue disorder resulting from in most parts of the world. About 10% of patients with
genetic defects in the genes coding for TGF-# recep- long-standing, untreated tertiary syphilis develop car-
tors.105,106 The characteristic features include arterial diovascular disease including aortic aneurysms.111 The
(especially aortic) aneurysms and dissections, global proximal portion of the aorta is the most extensively
arterial tortuosity, hypertelorism, bifid uvula, cleft lip, involved, leading to aortic dilation with mural calcifi-
and congenital heart disease. cation, aortic insufficiency, coronary artery stenosis, or
HIV-related vasculopathy is well known to affect frank aneurysm formation. Aneurysms usually are
medium- and small-caliber vessels. However, a rarer saccular and typically spare the aortic sinuses.
form of large vessel disease can cause solitary or multi- Infected aortic pseudoaneurysms can erode into
ple aneurysms in the aorta and its major branches.107,108 the respiratory or digestive system; likewise, inflam-
The disease produces a leukocytoclastic reaction in the matory or malignant mediastinal processes can de-
vasa vasorum and periadventitial tissues along with stroy the adjacent aortic wall. The end result may be an
chronic inflammation. The aneurysms often are saccular aortoenteric (e.g., aortoesophageal) fistula or aortobronchial
in appearance (Fig. 6-27). fistula. These devastating lesions classically present
with massive hematemesis or hemoptysis, respec-
tively.
Infectious Aortitis and
Despite the general prohibition of placing stent grafts
Aerodigestive Fistulas at sites of known infection, these devices have been
Bacterial aortitis is caused by seeding of an aortic lesion used in this setting to manage acute complications of
such as atherosclerotic plaque or a preexisting aneu- infectious aortic aneurysms. However, covered stent
rysm, septic embolization into the aortic vasa vaso- insertion should only be considered a temporizing
rum, transmural spread from an adjacent infection, or measure.112,113
6. THORACIC AORTA 149
A B
C D
FIGURE 6-29 Penetrating aortic ulcer. A and B, Axial and reformatted parasagittal contrast-enhanced chest computed tomography scans
show a very focal extension of contrast from the lumen into the wall of the mid-descending thoracic aorta (arrow). There is diffuse atheroscle-
rotic disease throughout the aorta. No frank dissection is seen. C, Patient underwent stent graft placement, which shows inflation of a large
balloon used to tack the device down to the aortic wall. D, Final aortogram shows exclusion of the ulcer with a widely patent lumen.
6. THORACIC AORTA 151
Intramural Hematoma more benign than with aortic dissection, but the mor-
In intramural hematoma (IMH), a localized hema- tality rate is still substantial (related to aneurysm rup-
toma develops spontaneously in the wall of the aorta ture or evolution to frank dissection, particularly with
without an intimal tear or overlying atherosclerotic type A lesions).114,126 Characteristics that favor complete
plaque.43,51,124,125 The postulated cause is rupture of resolution include type B lesion, younger age, diameter
aortic vasa vasorum; there is no proof for this prem- less than 4 cm, and thickness less than 1 cm.43,125,127
ise.114 Intramural hematoma is effectively a noncom- Many interventionalists advocate stent graft insertion
municating aortic dissection. It can progress to frank for the typical patient with type A IMH. Surgery or
dissection or rupture but fortunately is much less stent graft insertion usually is reserved for patients
likely to result in the malperfusion syndrome seen with with type B IMH and persistent symptoms, expansion
aortic dissection. IMH is being diagnosed more fre- of the hematoma, aortic diameter greater than 6 cm, or
quently with the widespread use of cross-sectional progression to frank dissection or rupture.49,128
imaging in patients with suspected aortic disease. The
clinical picture is similar to that of aortic dissection,
Coarctation of the Aorta (Online Case 27)
with sudden onset of chest or back pain in a middle-
aged to elderly hypertensive individual. Classic teach- Congenital thoracic aortic coarctation occurs in 0.02%
ing holds that intramural hematoma is a disease of to 0.06% of individuals.129 The obstruction takes
the descending thoracic aorta (type B). Some reports the form of a discrete bandlike narrowing at or
show a significant distribution in the ascending aorta beyond the attachment of the ligamentum arteriosum
(type A).124 (postductal form).130 This anomaly should not be con-
IMH usually is detected by CT or MRI, which shows fused with fetal coarctation, which produces diffuse
a crescentic mural hematoma of medium to high density narrowing of the aortic arch and hypoplasia of left
or signal intensity (depending on clot age) extending heart chambers (preductal form). Coarctation is asso-
over a length of the thoracic aorta115-117 (Fig. 6-30). There ciated with bicuspid aortic valve, patent ductus arte-
is no intimal flap nor flow within the collection. Intra- riosus, ventricular septal defect, and Turner syn-
mural hematoma must be differentiated from other drome. It usually is discovered in a child or young
diseases that cause wall thickening, such as aortitis, ath- adult with upper extremity hypertension, diminished
erosclerotic plaque, PAU, and mural thrombus. lower extremity pulses, or heart failure. To bypass the
IMH usually is treated by blood pressure and heart stenosis, blood flows from the anterior intercostal
rate control with beta-adrenergic blockers unless the branches of the internal thoracic arteries retrograde
ascending aorta is involved.125 The natural history is into the posterior intercostal branches of the descend-
ing aorta. Enlargement and tortuosity of the intercos-
tal arteries cause pressure erosion on the undersurface
of the third through ninth ribs (rib notching).
The characteristic findings of coarctation are severe
discrete narrowing around the aortic isthmus, dilation
of the ascending aorta, and enlarged internal thoracic
and intercostal arteries (Fig. 6-31). Operative treat-
ment of aortic coarctation is by direct resection with
end-to-end anastomosis or by patch aortoplasty.131
Balloon angioplasty and stent placement are attrac-
tive alternatives to surgery.132,133 Long-term results
are generally good, but restenosis or aneurysm for-
mation at the treatment site occurs in about 20% of
patients.
Pseudocoarctation of the aorta is a congenital elongation
of the thoracic aorta with a discrete kink at the aortic
isthmus.5 Although it looks superficially similar to true
coarctation, pseudocoarctation produces no pressure
gradient across the kink and has no collateral circulation
FIGURE 6-30 Intramural hematoma of the right lateral wall of (Fig. 6-32). Occasionally, aneurysms form adjacent to the
the ascending aorta on computed tomography angiogram. aortic twist.
152 II. AORTA AND PERIPHERAL ARTERIES
A B C
D E F
FIGURE 6-31 Coarctation of the aorta. A through C, Axial contrast-enhanced chest computed tomography images show that a short
segment of the proximal descending thoracic aorta is narrowed. The remainder of the visualized aorta looks normal. The internal thoracic
(mammary) arteries are prominent, as are multiple small posterior mediastinal vascular structures. D, The reformatted shaded-surface display
image confirms the diagnosis. E and F, A stent graft is placed with excellent cosmetic result.
A B
FIGURE 6-32 Pseudocoarctation of the aorta. A, Chest radiograph shows a rounded density (arrow) superior to the aortic knob.
B, Oblique parasagittal reformatted computed tomography angiogram shows marked kinking of the descending thoracic aorta but no
discrete stenosis. (Courtesy of Eric Goodman, MD, San Diego.)
6. THORACIC AORTA 153
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positive patients: another vasculitic enigma. Hum Pathol 2000;31:374. patients with type B aortic intramural hematoma. Circulation
109. Malouf JF, Chandrasekaran K, Orszulak TA. Mycotic aneurysms 2003;108:9.
of the thoracic aorta: a diagnostic challenge. Am J Med 2003;115:489. 128. Kaji S, Akasaka T, Horibata Y, et al. Long-term prognosis of
110. Oz MC, McNicholas KW, Serra AJ, et al. Review of Salmonella patients with Type A aortic intramural hematoma. Circulation
mycotic aneurysms of the thoracic aorta. J Cardiovasc Surg 1989;30:99. 2002;106(Suppl I):248.
111. Jackman Jr JD, Radolf JD. Cardiovascular syphilis. Am J Med 129. Mack G, Burch GH, Sahn DJ. Coarctation of the aorta. Curr Treat
1989;87:425. Options Cardiovasc Med 1999;1:347.
112. Lew WK, Rowe VL, Cunningham MJ, et al. Endovascular manage- 130. Tanous D, Benson LN, Horlick EM. Coarctation of the aorta:
ment of mycotic aortic aneurysms and associated aortoaerodi- evaluation and management. Curr Opin Cardiol 2009;24:509.
gestive fistulas. Ann Vasc Surg 2009;23:81. 131. Kaushal S, Backer CL, Patel JN, et al. Coarctation of the aorta:
113. Kan CD, Lee HL, Yang YJ. Outcome after endovascular stent graft midterm outcomes of resection with extended end-to-end anasto-
treatment for mycotic aortic aneurysm: a systematic review. mosis. Ann Thorac Surg 2009;88:1932.
J Vasc Surg 2007;46:906. 132. Egan M, Holzer RJ. Comparing balloon angioplasty, stenting, and
114. Sundt TM. Intramural hematoma and penetrating aortic ulcer. surgery in the treatment of aortic coarctation. Expert Rev Cardiovasc
Curr Opin Cardiol 2007;22:504. Ther 2009;7:1401.
115. Krishnam MS, Tomasian A, Malik S, et al. Image quality and 133. Kische S, Schneider H, Akin I, et al. Technique of interventional
diagnostic accuracy of unenhanced SSFP MR angiography repair in adult aortic coarctation. J Vasc Surg 2010;51:1550.
C H A P T E R
7
Abdominal Aorta
Karim Valji
AORTOGRAPHY The abdominal aorta has three ventral branches (Figs. 7-1
and 7-2). The celiac artery arises at the T12-L1 level. It can
Abdominal aortography is performed using a 4- or initially take a forward, upward, or dowward course. The
5-French (Fr) catheter with a pigtail or similar configu- superior mesenteric artery (SMA) takes off at the L1-L2 level
ration. To properly evaluate the renal artery origins, the about 1 cm below the celiac axis. The inferior mesenteric
side holes of the catheter are positioned at the L1-L2 artery (IMA) originates at the L3-L4 level, typically on the
level. When visualization of the celiac and superior left anterolateral surface of the aorta.
mesenteric arteries is necessary, higher catheter place- The paired inferior phrenic arteries classically originate at
ment (above the T12 level) is required. Lateral projec- or just above the celiac artery. They course superolaterally
tions are sometimes used to supplement frontal images toward the central tendon of the hemidiaphragms, where
in order to study the orifices of the mesenteric arteries. they bifurcate. Paired middle adrenal arteries take off from
Particular care should be taken when catheterizing the the aorta adjacent to the SMA to provide partial blood sup-
abdominal aorta in patients known to have aneurysms ply to the adrenal glands. The renal arteries originate just
or severe atherosclerotic disease to avoid dislodging
mural thrombus or plaque.
Inferior phrenic
Superior
ANATOMY mesenteric
Celiac
Development
In the embryo, the abdominal aorta is formed from the Renal
Middle
right and left dorsal aortae.1 Numerous ventral splanchnic adrenal
branches of the aorta supply the primitive digestive tract.
These channels are eventually reduced to the celiac, supe-
rior mesenteric, and inferior mesenteric arteries. Lateral
splanchnic branches supply organs arising from the meso-
nephric ridge, giving rise to the inferior phrenic, adrenal,
renal, and gonadal arteries. Four sets of somatic arterial Lumbar
branches evolve into the intersegmental lumbar arteries.
Inferior
mesenteric
Normal Anatomy
The abdominal aorta begins at the diaphragmatic hiatus.2
The vessel runs in front of the spine and to the left of Gonadal
the inferior vena cava (IVC) until it bifurcates into the
common iliac arteries at about the L4 vertebra. The normal
caliber of the abdominal aorta increases with age; at the
renal hila, its mean diameter varies from about 1.5 cm in Median
women in the fourth decade of life to about 2 cm in men sacral
in the eighth decade.3,4 FIGURE 7-1 Anatomy of the abdominal aorta.
156
7. ABDOMINAL AORTA 157
A B
CA
SMA
IMA
C D
FIGURE 7-2 Normal MR angiogram of the abdominal aorta in frontal (A) and lateral (B) reformations. C and D, Computed tomography
angiogram of the aorta in sagittal reformation. Ventral branches: CA, celiac artery; IMA, inferior mesenteric artery; SMA, superior mesenteric
artery.
below or at the level of the SMA. The gonadal (testicular or between these vessels, the lower intercostal arteries
ovarian) arteries are paired vessels off the anterolateral sur- (superiorly), and the iliolumbar, deep iliac circumflex,
face of the aorta just below the main renal arteries. and gluteal vessels (inferiorly). The median sacral artery
Four pairs of lumbar arteries exit the posterolateral takes off posteriorly just above the aortic bifurcation and
aspect of the aorta. There are extensive anastomoses descends toward the coccyx.
158 II. AORTA AND PERIPHERAL ARTERIES
FIGURE 7-3 Multiple renal arteries. Two renal arteries supply the
right kidney.
FIGURE 7-4 The common hepatic and splenic arteries have sepa-
rate origins from the abdominal aorta (straight arrows). Notice the right
The smaller somatic and splanchnic vessels (i.e., inferior hepatic artery replaced to the superior mesenteric artery (curved arrow).
phrenic, middle adrenal, gonadal, and median sacral
arteries) are not always seen on routine abdominal
aortograms. In a patient with an enlarged aorta or
Collateral Circulation
sluggish flow, the IMA may not opacify with a midab-
dominal aortic injection because of layering of con- With severe narrowing or complete occlusion of the
trast in the posterior (dependent) portion of the distal abdominal aorta, several parietal and visceral collateral
aortic lumen. pathways divert blood flow around the obstructed seg-
ment. The chief parietal collateral routes are from the
intercostal, subcostal, and lumbar arteries to the ilio-
Variant Anatomy lumbar, lateral sacral, and superior gluteal branches of
Congenital anomalies of the abdominal aorta are rare. the internal iliac artery and to the deep and superficial
However, anomalies of the primary branches are com- iliac circumflex branches of the external iliac artery
mon (see Chapters 10 and 11). Multiple renal arteries are (Fig. 7-5). With the latter system, blood flows through
present in about 25% to 35% of the population.5-7 the internal iliac artery to feed the external iliac artery
Although most accessory arteries are found just below in a retrograde direction. Interconnections between the
the main renal artery, they may arise above the main lumbar arteries help to support this collateral network.
trunk or as far distally as the iliac artery (Fig. 7-3). A pathway also exists from the superior epigastric ar-
Persistence of the embryonic ventral connection tery (terminal branch of the internal thoracic artery) to
between the celiac artery and SMA with regression of the inferior epigastric artery, which joins the common
the origin of one of these vessels leads to the rare celio- femoral artery.
mesenteric artery8 (see Fig. 11-10). The hepatic, left gas- The SMA and IMA are critical visceral conduits when
tric, or splenic arteries may have a separate origin the abdominal aorta is obstructed. With occlusion of the
from the aorta (Fig. 7-4). The inferior phrenic arteries aorta above the level of the IMA, the SMA feeds the IMA
can exit the top of the celiac (or rarely a renal) artery or through the middle colic and marginal arteries, which
form a common trunk from the aorta.9,10 Rarely, a pair then connect with branches of the internal iliac artery
of lumbar arteries arise as a single branch from the through the rectal network (see Fig. 11-15). With occlu-
posterior aspect of the aorta. sion of the abdominal aorta below the IMA origin, the
7. ABDOMINAL AORTA 159
A D
B C E
FIGURE 7-5 Distal aortic occlusion encompassing the superior mesenteric artery (SMA). A and B, Early and late phase frontal
aortography show complete occlusion below the IMA (large arrow). A huge plaque obstructs the SMA origin (curved arrow), which is
fed largely through celiac artery collaterals (small arrow). The IMA (white arrow) is huge, as are subcostal arteries headed toward the
pelvis (arrowheads). The left renal artery is patent, but the right renal artery is severely diseased and feeds a small kidney. C, Lateral
aortography also shows a tight celiac artery stenosis (arrow) and SMA occlusion. D and E, Pelvic imaging shows reconstitution of the
internal iliac arteries (arrows) through the rectal network from the distal IMA (arrowheads). Parietal arteries also assist in diverting blood
around the occlusion.
rectal collateral network (between the superior rectal Degenerative Abdominal Aortic Aneurysms
branch of the IMA and the middle and inferior rectal (Online Cases 14 and 65)
branches of the internal iliac artery) may be an impor-
tant communication (see Fig 7-5). In cases of short- Etiology
segment aortic stenosis involving the SMA, the so- An arterial aneurysm is defined as a localized dilation
called meandering mesenteric artery can fill the SMA of the vessel by 50% or more of its normal diameter.12,13
from the IMA circulation11 (see Fig. 11-16). By general agreement, an abdominal aortic aneurysm
(AAA) is present in an adult when the wall-to-wall
diameter of the infrarenal aorta exceeds 3 cm.14 Most
MAJOR DISORDERS AAAs are infrarenal; in large series, up to 15% are
suprarenal or juxtarenal (extending !1 cm from the
renal arteries).15-17 More than 20% of abdominal aneu-
Atherosclerosis rysms extend into one or both common iliac arteries.
Atherosclerosis is the most common disease affecting the The incidence of AAA has risen significantly during
abdominal aorta (Fig. 7-6). This condition is considered the last half century, and this phenomenon cannot be
as part of lower extremity peripheral vascular disease in attributed entirely to earlier detection through screen-
Chapter 8. ing or aging of the population.18,19
160 II. AORTA AND PERIPHERAL ARTERIES
BOX 7-1
C AU S E S O F A B D O M I N A L
A O RT I C A N E U RY S M S
Degeneration (atherosclerosis-associated)
Inflammation
Chronic dissection with aneurysm formation
Infection (mycotic aneurysm)
Trauma
Vasculitis
Noninflammatory vasculopathy
Connective tissue disorders
Congenital disorders
A B
organs, aneurysm thrombosis, distal embolization, or saccular or eccentric without calcification or adjacent
dissection. The rare patient with an aortocaval fistula aortic disease, or is present in a young patient, un-
may exhibit pain, a pulsatile abdominal mass, continu- common causes should be considered (see Box 7-1).
ous abdominal bruit or thrill, congestive heart failure, CTA is the best means for evaluating patients with sus-
lower extremity edema, or hematuria. pected AAA rupture.45,47-49 Acute aneurysm rupture pro-
duces strandlike soft tissue density with high attenuation
Imaging in the retroperitoneum adjacent to the aneurysm (often
Before considering invasive treatment, imaging studies posteriorly) (Fig. 7-9). It may be difficult to pinpoint the
are necessary for AAA detection and staging, surveil- exact site of leak. Several CT findings have been described
lance of small aneurysms, and diagnosis of rupture or as suggestive of impending aortic rupture, including
other complications. a high-attenuation crescent sign within or between the
luminal thrombus and the aortic wall.
SONOGRAPHY Other entities can mimic acute aneurysm leak, in-
Ultrasound (US) is the chief tool for detecting, sizing, cluding chronic rupture, perianeurysmal fibrosis from
and monitoring AAAs35 (Fig. 7-7). The technique is an inflammatory aneurysm (see later), lymphadenopathy,
almost 100% sensitive for aneurysm diagnosis. Body unopacified duodenum, and spontaneous retroperito-
habitus or overlying structures (e.g., bowel gas) makes neal hemorrhage (Fig. 7-10).
the test useless in some individuals. There is strong
evidence that US screening programs in populations at
risk will reduce overall mortality attributable to this
lethal disease.35,37 Sonography also is highly accurate
in determining aneurysm size, the presence of mural BOX 7-2
thrombus, and associated abdominal pathology. US
is less accurate in assessment of the cranial and caudal IMAGING OF ABDOMINAL
extent of the aneurysm, the relationship to and num- A O RT I C A N E U RY S M S
ber of renal arteries, and the presence of iliofemoral B E F O R E R E PA I R
arterial disease.
Proximal and distal extent of aneurysm
COMPUTED TOMOGRAPHY (including extension to iliac arteries)
Computed tomography angiography (CTA) is the Number, location, and patency of renal arteries
principal modality for preprocedure and postproce- Presence of obstructive iliofemoral arterial
dure assessment of patients with AAA43-46 (Box 7-2). disease
CT also is useful in following aneurysm growth in Patency of mesenteric arteries
patients who cannot be imaged adequately with sonog- Presence of associated anomalies or pathology
raphy. In those with underlying renal dysfunction, (e.g., horseshoe kidney)
the need for iodinated contrast material is a major Presence of inflammatory aneurysm
drawback of CTA. Evidence of rupture
The typical AAA is a fusiform dilation of the infra- Presence of inferior vena cava or renal vein
renal abdominal aorta (Fig. 7-8). Intimal calcification anomalies
and mural thrombus are common. If the aneurysm is
162 II. AORTA AND PERIPHERAL ARTERIES
C E
A C D
E F
FIGURE 7-9 Acute rupture of an abdominal aortic aneurysm (AAA). Unenhanced axial (A and B) and contrast-enhanced reformatted
coronal (C) CT images show a huge AAA that ends above the aortic bifurcation. There is high-density, heterogeneous soft tissue to the right
of the aneurysm that represents recent leak (arrows). D, E, and F, A stent-graft is being inserted emergently to treat the ruptured aneurysm.
inhibitors (statins) will slow the progression of AAA Of course, the benefits of watchful waiting with
expansion.56 The sole purpose of invasive AAA inter- imaging surveillance in a particular individual must
vention is to prevent rupture. be weighed against the operative mortality rate for
elective open or endovascular AAA repair (!5%) and
PATIENT SELECTION the high mortality rate associated with ruptured AAAs
There is general agreement among vascular interven- (50% to 75%).36,39 Risk factors for rupture include
tionalists that all AAA larger than 5 cm in transverse female gender, advanced age, and continued smoking.
wall-to-wall diameter should be repaired electively The indications for open versus endovascular repair
and that smaller asymptomatic aneurysms be routinely are evolving but are based primarily on anatomic
followed by imaging studies.33-37 Smaller AAAs are factors, comorbid conditions, and patient/physician
considered for repair if they are symptomatic (causing preference. Endovascular AAA repair (EVAR) with
pain, tenderness, or distal embolization) or enlarging a stent graft should certainly be considered in pa-
rapidly (%5 mm/6 months). tients with advanced age, significant operative risk, or
164 II. AORTA AND PERIPHERAL ARTERIES
A B
7. ABDOMINAL AORTA 165
A B C
D E F
FIGURE 7-15 Internal iliac artery embolization prior to EVAR. A, Contrast-enhanced CT scan shows a large internal iliac artery aneurysm
with extensive mural thrombus and intimal calcification (large arrow). Right internal iliac artery is dilated and calcified (small arrow). B and
C, Catheter angiography outlines the aneurysm and branches beyond (arrows). These distal branches must be excluded first with multiple coils
(D and E) to prevent backfilling of the aneurysm before more proximal embolization with an Amplatzer plug (F, arrow). Lesion is now
completely excluded from the circulation.
7. ABDOMINAL AORTA 169
Material Nitinol, polyester Nitinol, ePTFE SS, polyester Nitinol, polyester Co-Ch, ePTFE
Design 2-piece, bifurcated 2-piece, modular 3-piece, modular 2-piece, bifurcated Unibody, bifurcated
Proximal fixation Infrarenal Infrarenal Suprarenal Suprarenal Infrarenal
Diameters 20-28 mm 22-31 mm 22-36 mm 22-36 mm 25-34 mm
Lengths 13.5-16.5 cm 12-18 cm 8.2-14 cm 15.5-18.5 cm 12-17.5 cm
Iliac limb diameter 12-20 mm 12-20 mm 8-24 mm 10-22 mm 16 mm
Aortic sheath 19, 21 Fr 18 Fr 18-22 Fr 21 Fr
Iliac sheath 16-19 Fr 12 Fr 14, 16 Fr 9 Fr
Co-Ch, cobalt chromium alloy; ePTFE, expanded polytetrafluoroethylene; Fr, French; SS, stainless steel.
B C
A
FIGURE 7-16 Endografts for abdominal aortic aneurysms. A, Zenith endograft. B, Excluder device, main module expanded (top) and
wrapped (bottom) on deployment catheter. C, Excluder device with iliac limb extension in place. (A, Courtesy of Cook, Inc; B and C, Courtesy
of W. L. Gore and Associates.)
Type I endoleak is defined as failure at the proximal or Fig. 7-18). Grafts are salvaged by transarterial balloon dila-
distal component attachment sites, most often inferior tion of leaky attachment sites or insertion of an additional
migration of the proximal stent and/or neck dilation101 stent graft cuff. Sometimes, the leak is sealed with glue
(Fig. 7-18). Neck dilation is known to progress over time or coils.75 Conversion to open repair is rarely necessary.
after open aneurysm repair, but the surgical construc- Type II endoleak is by far the most common late event
tion precludes leak. The behavior of the neck after EVAR after EVAR. In this situation, blood flows in a retro-
depends to some extent on the self-expanding or bal- grade direction through an aortic sac side branch and
loon-expandable nature of the proximal component.79 then must exit the aneurysm sac through the same
CT scans show hyperdense blood in the sac before con- vessel (simple) or another branch (complex). The
trast injection and focal extravasation contiguous with lumbar arteries, IMA, or internal iliac artery (typically the
an attachment site after contrast.102 Duplex ultrasound iliolumbar branch) are the usual culprits. Rarely, an
may depict the flow stream at this site. accessory renal or median sacral artery is responsible
Type III endoleak refers to delayed loss of integrity of (Figs. 7-20 and 7-21). Contrast-enhanced CT shows
an individual component stent or fabric. On CT im- focal extravasation in the sac away from the graft it-
ages, the focal contrast collection does not correspond self and usually remote from the device attachment
to attachment sites. In a summary of published series, points.102 The leak may not be evident on the aorto-
mean frequency of delayed type I and III endoleaks were gram or selective arteriogram; superselective studies
6% and 1%, respectively. All type I and type III endoleaks (e.g., microcatheterization of the marginal artery or the
require treatment upon detection (Fig. 7-19 and see iliolumbar arterial collateral into a lumbar artery) are
170 II. AORTA AND PERIPHERAL ARTERIES
sometimes required75 (see Fig. 7-20). Many type II Therefore the following subset of patients should be
endoleaks resolve spontaneously, so observation and considered for treatment.35,76,103-105
imaging follow-up is often sufficient. If the aneurysm
Persistent type II endoleak (%6 months)
sac does not grow, most others have a benign course.
Type II endoleak with aneurysm expansion
However, aneurysm rupture in patients with this type
of endoleak has been reported, and new endoleak has There is still controversy regarding endoleak closure
been discovered many years after the procedure. with persistent leak without sac expansion.106,107
A B C
D E F G
FIGURE 7-17 Steps in EVAR placement. A through C, Contrast-enhanced axial and lateral and frontal shaded surface display CT
angiograms demonstrates a large infrarenal abdominal aortic aneurysm (AAA). D, Diagnostic aortography following bilateral femoral
artery access. E, The main stent graft module is in place. F, Main module is deployed. G, Left iliac component in place.
7. ABDOMINAL AORTA 171
H J K
FIGURE 7-17, contd H, Final aortogram shows exclusion of the aneurysm. I through K, Follow-up axial and shaded surface display
reformatted images show complete exclusion of AAA afterward with no evidence for endoleak. A postprocedure right renal infarct is
identified.
C D
or micropuncture system is inserted about one Type IV endoleak was a transient feature of older de-
hand breadth from the midline toward the left vices with more porous fabric material that allowed
lateral border of the spine from the left flank early seepage of blood. They never required treatment.
(or right flank if a transcaval approach is Type V endoleak (endotension) refers to aneurysm
deemed necessary).115 Once the aneurysm sac growth after EVAR with persistent pressurization of
is entered, the pressure is measured and the sac the sac without a detectable endoleak.117 The etiology
is embolized with cyanoacrylate and/or coils for this phenomenon is somewhat obscure, but is per-
(Fig. 7-22). Great care should be taken to prevent haps caused by a leak below the threshold for current
glue from backfilling into the IMA circulation. imaging detection or persistent transgraft pressure
Thrombin has been used is this setting, but (rather than flow) on the native aortic wall. Aneurysm
serious visceral injury has occurred.116 rupture is theoretically possible. Endovascular meth-
Laparoscopic branch ligation. ods may be used to treat this condition, and open
7. ABDOMINAL AORTA 173
A B
TABLE 7-3 Endoleak Classification Thrombosis also may occur in the setting of less com-
mon entities that narrow the aorta.
Type Definition
Box 7-5 outlines the major causes for acute abdomi-
I Attachment leak or failure nal aortic occlusion.119,120 About 50% to 65% of cases
IA Proximal end result from embolism.121 Thrombosis of AAAs often
IB Distal end
IC Iliac component
follows disruption of mural thrombus followed by
II Retrograde branch flow into aneurysm sac distal embolization.122 In many cases, distal aortic oc-
IIA Simple (single inflow/outflow vessel) clusion propagates back toward the level of the renal
IIB Complex (multiple inflow/outflow vessels) arteries or SMA. The ultimate level of the occlusion is
III Device deterioration or dehiscence distributed about evenly above and below the origin
IIIA Disruption of modular stent components
IIIB Fabric defect
of the IMA.
IIIC Other defect
IV Graft porosity Clinical Features
V Endotension Most patients with chronic aortic occlusion have a long
history of smoking. Symptoms and signs depend largely
on whether the occlusion is acute or chronic. Patients
with acute occlusion may have sudden onset of bilateral
repair is rarely necessary. Future modifications in graft lower extremity rest pain, absent pulses, cool and mot-
material may ultimately prevent this perplexing, un- tled skin, and neurologic deficits. Prior episodes of
common problem. myocardial infarction or cardiac dysrhythmias are com-
mon. Patients with chronic occlusion usually complain
Aortic Occlusive Disease (Online Case 42) of severe, progressive, bilateral leg claudication, along
with impotence in some men. Distal leg pulses often are
Etiology diminished or absent. However, with good collateral
Complete occlusion of the abdominal aorta can present circulation, weak femoral pulses may be palpable in
as an acute or chronic event. The most common cause of patients with complete long-standing occlusion.
chronic occlusion is thrombosis superimposed on severe
atherosclerosis of the distal abdominal aorta and com- Imaging
mon iliac arteries. The Leriche syndrome describes such Acute and chronic occlusions are imaged with CT or
patients with buttock and thigh claudication, impotence, MR angiography. When catheter arteriography is per-
thigh muscle atrophy, and diminished femoral pulses.118 formed (usually because endovascular treatment is
174 II. AORTA AND PERIPHERAL ARTERIES
A B
C D E
FIGURE 7-20 Type II endoleak following endovascular aneurysm repair. A and B, Contrast-enhanced computed tomography scans show
filling of both iliac limbs of the aortic graft. Extravasation of contrast into the anterior portion of mural thrombus (arrow) indicates endoleak,
probably from the inferior mesenteric artery (IMA). C, The superior mesenteric artery was catheterized. A coaxial microcatheter was negotiated
into the middle colic artery, then the marginal artery and finally the left colic branch of the IMA. D, The microcatheter was advanced further
through the IMA root and directly into the aneurysm sac, into which contrast spills. E, Coils were deposited back from the sac into the
proximal IMA, closing the endoleak.
Treatment
contemplated), a left brachial artery approach is recom-
mended. However, it may be possible to enter the SURGICAL THERAPY
femoral artery using ultrasound guidance and traverse Historically, the mortality for patients with acute abdomi-
the occlusion with a hydrophilic guidewire, even with nal aortic occlusion was greater than 50%.121 Patients with
faint or absent pulses. The catheter should be advanced embolic aortic obstruction are treated with embolectomy in
carefully into the abdominal aorta to within several many cases.120,121 For acute or chronic thrombotic occlusion,
centimeters of the site of occlusion. aortobifemoral bypass grafting is the procedure of choice.
Chronic occlusion invokes an extensive collateral
circulation (see Fig. 7-5). A filling defect in the aorta in- ENDOVASCULAR THERAPY
dicates acute embolism or in situ thrombosis. Involve- Interventional radiology has a role in the management
ment of the renal or mesenteric arteries should be of chronic aortic occlusion, particularly when disease is
sought. Rarely, extension of a thoracic aortic dissection isolated to the distal portion of the abdominal aorta.123-125
causes acute abdominal aortic occlusion. Thrombolysis (to lyse fresh clot), angioplasty, and intra-
7. ABDOMINAL AORTA 175
B C
FIGURE 7-21 Type II endoleak in a patient lost to follow-up years after stent-graft placement. A, Computed tomography angiogram
shows huge abdominal aortic aneurysm displaced to the right with patent endograft and contrast extravasation into clot, indicating endoleak.
B, Early phase of catheter aortogram reveals a widely patent device. C, Late phase shows leak into aneurysm sac through internal iliac artery
branches (arrow) feeding a right lumbar artery in a retrograde direction (curved arrow). (Courtesy of Anne C. Roberts, MD, San Diego, Calif.)
B C
FIGURE 7-22 Recurrent type II endoleak treatment by translumbar embolization. Patient had type II endoleak treated 2 years earlier.
A, Computed tomography angiogram shows persistent leak into aneurysm sac. B, Following translumbar catheter placement, there is antegrade
filling of bilateral lumbar arteries. C, Multiple coils and x-butyl cyanoacrylate were used to fill the sac. (Courtesy of William Stavropoulos,
Philadelphia, Pa.)
BOX 7-6
BOX 7-5 C AU S E S O F A B D O M I N A L
A O RT I C N A R R O W I N G
C AU S E S O F A C U T E
OCCLUSION OF THE Atherosclerosis
A B D O M I N A L A O RTA Dissection
Aneurysm with mural thrombus
Embolism (usually cardiac source) Vasculitis
Thrombosis superimposed on atherosclerotic Takayasu arteritis
disease Congenital coarctation syndromes
Thrombosis of abdominal aortic aneurysm Neurofibromatosis
Trauma Williams syndrome
Iatrogenic injury (e.g., catheterization) Congenital rubella
Thrombophilic state Tuberous sclerosis
Dissection Middle aortic syndrome
Extrinsic compression Radiation aortitis
7. ABDOMINAL AORTA 177
C D
wall.129,130 Genetic factors also have been implicated, regression of periaortic inflammation (65%) compa-
including an association with the human leukocyte rable to open repair.136
antigen molecule and autoimmune diseases.131
Inflammatory aneurysms account for about 3% to
Infectious Aortic Aneurysms
10% of all AAAs.40,132,133 Compared with patients with
degenerative aortic aneurysms, this subgroup is some- Infectious (mycotic) aneurysms or pseudoaneurysms are
what younger, more likely to be male, and more often caused by local seeding of diseased vessel wall (usually
symptomatic at presentation, but much less likely to atherosclerotic plaque), seeding through the vasa vaso-
rupture (lifetime risk $5%).40 Patients may have fever, rum, direct invasion from an adjacent infection, or
weight loss, and an elevated erythrocyte sedimentation penetrating trauma. Mycotic aneurysms account for
rate or C-reactive protein during the acute phase of the about 1% to 2% of all AAA.137 They are especially
illness. Abdominal or back pain is much more common lethal, with a substantial risk for rapid growth, rupture,
in patients with inflammatory aneurysms than in those and postoperative mortality138 Among the more com-
with degenerative ones. mon offending organisms are Staphylococcus aureus and
On CT or MRI, the diagnosis is suggested by a smooth, Salmonella species.137,139 Mycobacterial AAA are also
confluent rind of enhancing soft tissue around the described.140 The thoracoabdominal and abdominal
anterior and lateral margins of the aorta134,135 (Fig. 7-24). aorta are more commonly affected than the thoracic
The posterior border of the aorta often is spared. In- aorta. Most patients are intravenous drug abusers or
volvement of the small bowel, ureters, or IVC in the alcoholics, or are immunocompromised.
fibrotic process is characteristic. These features usually Abdominal or back pain, fever, a pulsatile mass, ele-
allow distinction from aortic rupture, metastatic disease, vated inflammatory markers (such as C-reactive protein
or lymphadenopathy (see Figs. 7-9 and 7-10). Identifica- and white blood cell count), and positive blood cultures
tion of disease in adjacent organs is important before may be present. The diagnosis is confirmed by cross-
invasive treatment. sectional imaging. The typical finding is a saccular, eccen-
Most practitioners opt for a course of corticosteroids tric aneurysm, usually with little or no adjacent aortic
in the acute phase of the illness.40 However, aneurysm disease141 (Fig. 7-25). Enhancing periaortic soft tissue
repair appears to halt (and even reverse) the inflamma- may be evident. Multiple aneurysms are common.
tory process. Recently, EVAR has been used in this Patients are treated vigorously with intravenous
condition with perioperative mortality (about 2%) and antibiotics. If the patient does not undergo surgical
178 II. AORTA AND PERIPHERAL ARTERIES
B C
FIGURE 7-24 Inflammatory abdominal aortic aneurysm. A through C, Contrast-enhanced computed tomography scan shows the
aortic aneurysm with a large rind of soft tissue around the anterolateral portion of the aorta. The inflammatory mass entirely surrounds
the common iliac arteries. The inferior vena cava is obliterated by the mass, and a bowel loop has become enmeshed within it (short arrow).
Left hydronephrosis (long arrow) indicates that at least the left ureter is involved.
Trauma
Injury to the abdominal aorta occurs from accidental,
FIGURE 7-25 Mycotic aneurysm of the distal abdominal aorta on criminal, or iatrogenic penetrating trauma and, less
gadolinium-enhanced magnetic resonance angiogram. commonly, from blunt trauma.149-151 Penetrating injuries
7. ABDOMINAL AORTA 179
A B
FIGURE 7-26 Takayasu arteritis. A, Typical smooth long-segment infrarenal aortic narrowing in a 7-year-old girl (lateral projection of
abdominal aortogram). B, Atypical aortic and iliac artery aneurysms in another young girl.
180 II. AORTA AND PERIPHERAL ARTERIES
60. Cambria RP, Brewster DC, Abbott WM, et al. Transperitoneal versus 83. Turnbull IC, Criado FJ, Sanchez L, et al. Five-year results for the
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78. Tan JWC, Yeo KK, Laird JR. Food and Drug Administration ap- aneurysm surveillance following endovascular aneurysm repair:
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79. Chuter TAM. Durability of endovascular infrarenal aneurysm 101. Stavropoulos SW, Baum RA. Imaging modalities for the detection
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80. Greenberg RK, Sternbergh III WC, Makaroun M, et al. Intermediate cular abdominal aortic aneurysm repair: management strategies
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7. ABDOMINAL AORTA 183
105. Faries PL, Cadot H, Agarwal G, et al. Management of endoleak 128. Trimarchi S, Tsai T, Eagle KA, et al. Acute abdominal aortic dis-
after endovascular aneurysm repair: cuffs, coils, and conversion. section: insight from the International Registry of Acute Aortic
J Vasc Surg 2003;37:1155. Dissection (IRAD). J Vasc Surg 2007;46:913.
106. Jones JE, Atkins MD, Brewster DC, et al. Persistent type 2 endoleak 129. Rasmussen TE, Hallett Jr JW. Inflammatory aortic aneurysms. A
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107. Bernhard VM, Mitchell RS, Matsumura JS, et al. Ruptured abdomi- 130. Vaglio A, Corradi D, Manenti L, et al. Evidence of autoimmunity
nal aortic aneurysm after endovascular repair. J Vasc Surg 2002; in chronic periaortitis: a prospective study. Am J Med 2003;114:454.
35:1155. 131. Haug ES, Skomsvoll JF, Jacobsen G, et al. Inflammatory aortic
108. Silverberg D, Baril DT, Ellozy S, et al. An 8-year experience with aneurysm is associated with increased incidence of autoimmune
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a safe approach. J Vasc Surg 2006;44:453. 132. Leseche G, Schaetz A, Arrive L, et al. Diagnosis and management
109. Baum RA, Carpenter JP, Stavropoulos SW, et al. Treatment of type of 17 consecutive patients with inflammatory abdominal aortic
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rysms: comparison of transarterial and translumbar techniques. 133. Di Marzo L, Sapienza P, Bernucci P, et al. Inflammatory aneurysm
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112. Baum RA, Cope C, Fairman RM, et al. Translumbar embolization 136. Paravastu SC, Ghosh J, Murray D, et al. A systematic review of
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C H A P T E R
8
Pelvic and Lower Extremity Arteries
Karim Valji
185
186 II. AORTA AND PERIPHERAL ARTERIES
Iliolumbar
artery
Common
iliac
artery
Inferior epigastric
artery
Common femoral
artery
Obturator
artery
A B
Inferior gluteal Internal
artery pudendal artery
Common
femoral
artery
Deep femoral
artery
Lateral femoral
circumflex
artery
Medial
femoral
circumflex
artery
Superficial
femoral
artery
C D
FIGURE 8-1 Normal pelvic and left lower extremity arteriograms. A, The abdominal aorta divides into the common iliac arteries at the L4-L5
level. B, The branching pattern of the internal iliac artery varies. C, The common femoral artery divides into the superficial femoral artery (SFA)
and deep femoral artery near the bottom of the femoral head. D, The SFA passes down the anteromedial aspect of the thigh, dives into the flexor
muscle compartment, and runs through the adductor (Hunter) canal.
8. PELVIC AND LOWER EXTREMITY ARTERIES 187
Superior
geniculate
artery
Peroneal Anterior
artery tibial
artery
Sural
artery
Popliteal Posterior
artery tibial
artery
Lateral
Anterior
tarsal
tibial
artery
artery
Posterior Dorsalis
Anterior tibial pedis
tibial artery artery
artery
Medial
plantar
Posterior
artery
tibial
artery Lateral
Peroneal plantar
artery artery
E F G
FIGURE 8-1, contd E and F, At the distal border of the popliteus muscle, the popliteal artery divides. G, The dorsalis pedis artery gives
off medial and lateral tarsal branches. The posterior tibial artery gives off medial and lateral plantar branches.
A B C D
FIGURE 8-2 Pelvic and lower extremity maximum intensity projection magnetic resonance angiogram. Pelvis in frontal (A) and near
lateral (B) views. Thigh (C) and calf (D) in frontal view. The right anterior tibial artery is occluded in the upper calf (arrow).
188 II. AORTA AND PERIPHERAL ARTERIES
the internal iliac artery is quite variable (see Fig. 8-1B). arteries, all of which form an anastomotic network
Classically, the major branches of the anterior division around the knee.
are as follows: At the distal border of the popliteus muscle, the pop-
liteal artery divides.7 The anterior tibial artery arises later-
Obturator artery
ally, pierces the interosseous membrane, and then runs
Internal pudendal artery, which supplies the
in front of the lower tibia (see Fig. 8-1E and F). It passes
external genitalia and rectum (see Fig. 13-11)
over the ankle onto the dorsum of the foot to become the
Inferior gluteal artery, which nourishes muscles
dorsalis pedis artery. The tibioperoneal trunk is the direct
of the thigh and buttocks and the sciatic nerve
continuation of the popliteal artery and bifurcates just
Visceral arteries, which supply the bladder,
beyond its origin into the posterior tibial and peroneal
rectum, and uterus or prostate through the
arteries. The posterior tibial artery runs posteriorly and
superior and inferior vesicular, middle rectal,
medially in the flexor compartment. The peroneal artery
and uterine or prostatic arteries, respectively
runs between the posterior and anterior tibial arteries
(see Fig. 13-16). They may be hard to identify
near the fibula. It is a small-caliber vessel unless func-
on a routine pelvic arteriogram.
tioning as a collateral in the face of tibial artery obstruc-
The major branches of the posterior division of the tion. In the distal calf, its perforating and communicat-
internal iliac artery are: ing branches may join the anterior and posterior tibial
arteries, respectively. Above the ankle, the artery divides
Iliolumbar artery, which takes off laterally to
into two calcaneal branches (fish tail) that have anas-
supply the lumbar muscles
tomoses with the distal tibial arteries.
Lateral sacral artery, which takes off medially
A network of malleolar arteries interconnect the tibial
toward the sacral foramina
arteries above the ankle.7 The dorsalis pedis artery gives
Superior gluteal artery, which is the largest
off medial and lateral tarsal branches (see Fig. 8-1G). The
branch of the division and feeds the gluteal
posterior tibial artery passes behind the medial malleo-
muscles
lus, where it divides into medial and lateral plantar ar-
At the junction of the external iliac and common teries. The plantar arch is formed by the dominant lateral
femoral arteries (which corresponds to the inguinal plantar branch of the posterior tibial artery and the dis-
ligament), the inferior epigastric artery exits medially tal dorsalis pedis artery. Smaller secondary arches are
(see Fig. 3-1). It runs alongside the rectus abdominis created by other branches of the distal tibial arteries.
muscle before communicating with the superior epigas- Metatarsal arteries arise primarily from the plantar arch.
tric branch of the internal thoracic (mammary) artery.
The deep iliac circumflex artery takes off laterally and
Variant Anatomy (Online Case 102)
superiorly (see Fig. 3-5).
The common femoral artery (CFA) courses over the The most common variations in branching of the inter-
femoral head encased in the femoral sheath along with nal iliac artery involve anomalous origin of a named
the femoral vein (medial or posteromedial) and the fem- artery (e.g., obturator, inferior gluteal, or superior glu-
oral nerve (lateral). Branches of the CFA include the teal) from another major branch of either division.
superficial epigastric artery, superficial circumflex iliac The persistent sciatic artery is a rare anomaly (about
artery (laterally), and external pudendal artery (medi- 0.1% of the population) in which the embryologic sciatic
ally); all of these are inconsistently seen at angiography. artery remains the dominant inflow vessel to the leg.8,9
The CFA divides into the superficial femoral artery (SFA) The aberrant vessel arises from the internal iliac artery,
and deep femoral artery (DFA) or profunda femoris artery passes through the greater sciatic foramen, and lies deep
(PFA) near the bottom of the femoral head (see Fig. 8-1C). to the gluteus maximus muscle (Fig. 8-3). Above the
A high bifurcation is occasionally seen. The DFA takes knee, it joins the popliteal artery. The SFA is hypoplastic
off laterally and posteriorly. Its major branches are the or absent. The anomaly is occasionally bilateral. Because
lateral femoral circumflex, medial femoral circumflex, of its relatively superficial position in the ischial region,
and four or so pairs of perforating arteries. the sciatic artery is prone to intimal injury or aneurysm
The SFA passes down the anteromedial aspect of formation.
the thigh, dives into the flexor muscle compartment, Very rare femoral artery variants include the saphe-
and runs through the adductor (Hunter) canal (see nous artery and duplication of the SFA.10 Anomalies of the
Fig. 8-1D). The SFA then becomes the popliteal artery, DFA are common, including a posterior or even medial
which is posterior to the femur (surrounded by the heads origin of the main DFA trunk and separate origins of the
of the gastrocnemius muscle) and deep to the popliteal medial and lateral circumflex femoral branches.
vein. Its major muscular branches are the sural arteries Tibial artery anomalies are present in about 3% to 10% of
and paired superior, middle, and inferior geniculate the population.11-13 The variants often are bilateral. The
8. PELVIC AND LOWER EXTREMITY ARTERIES 189
iliolumbar arteries, DFA to the gluteal arteries
through femoral circumflex branches
External iliac artery obstruction: posterior
division of the internal iliac artery branches to
the CFA through the deep iliac circumflex artery,
anterior division of the internal iliac artery
branches to circumflex femoral branches of DFA,
transpelvic collaterals
SFA obstruction: collaterals depend on the site
and length of the obstruction; the DFA becomes the
dominant route to the lower leg, with lateral
femoral circumflex and perforating vessels
supplying branches of the distal SFA and popliteal
arteries
DFA obstruction: internal iliac artery branches to
medial and lateral circumflex femoral branches of
the DFA
Popliteal artery obstruction: geniculate and sural
collateral networks
Tibial artery obstruction: the peroneal artery is
the principal collateral channel with anterior or
posterior tibial artery obstruction
FIGURE 8-3 Bilateral persistent sciatic arteries. Maximum inten-
sity projection MR angiogram shows a large vessel arising from each
internal iliac artery (arrows) passing laterally over the femoral heads
and running down the legs lateral to the expected position of the MAJOR DISORDERS
femoral arteries.
C D
8. PELVIC AND LOWER EXTREMITY ARTERIES 191
A B
C D
FIGURE 8-5 Collateral patterns in cases of lower extremity arterial obstructions (see text for details). A and B, Right common iliac ar-
tery (CIA) occlusion with major collateral circulation through the fourth lumbar artery (black arrow) to the iliolumbar branch of the internal
iliac artery (IIA, white arrow) and then into the external iliac artery (EIA, curved arrow). There are also transpelvic collaterals from left to right
IIA (double white arrows). Note renal transplant off the right EIA. C, Bilateral IIA occlusions. In addition to distal external iliac/common
femoral collaterals, the enlarged inferior mesenteric artery (arrow) contributes to the IIA branches. D, Right external iliac artery occlusion
with reconstitution of the proximal deep femoral artery (arrow). Continued
192 II. AORTA AND PERIPHERAL ARTERIES
E F G
I J
FIGURE 8-5, contd E, Left femoropopliteal and proximal tibial artery occlusions. Deep femoral branches reconstitute a short segment of
the midpopliteal artery, which supplies sural collaterals (arrow) into the calf. The posterior tibial artery is reconstituted in the midcalf. F, Critical
stenosis of distal right superficial femoral artery (arrow) with multiple collateral channels. G, Posterior and anterior tibial artery occlusion, with
the peroneal artery reconstituting the distal vessels in the foot. H through J, Thrombosis of left limb (long white arrow) of aortobifemoral bypass
graft on axial and reformatted coronal contrast enhanced computed tomography images. The left leg is partially fed through superficial epigas-
tric branches (arrowheads) of the distal left internal thoracic (mammary) artery. These vessels communicate with branches of the inferior epigas-
tric artery (black arrow) which then fill the left common femoral artery.
8. PELVIC AND LOWER EXTREMITY ARTERIES 193
C AU S E S O F L O W E R R I S K FA C T O R S F O R
EXTREMITY PERIPHERAL P E R I P H E R A L A RT E R I A L
A RT E R I A L D I S E A S E DISEASE
Atherosclerosis Diabetes
Thrombotic occlusion of underlying stenosis Insulin resistance without diabetes
Embolism Smoking
Thromboembolism Hypertension
Microembolization Dyslipidemia (especially elevated total/high
Trauma density lipoprotein cholesterol)
Catheterization Thrombophilic states (see Boxes 1-4 and 1-5)
Aneurysm Age
Thrombosis (e.g., popliteal artery) Non-white race
Distal embolization
Neointimal hyperplasia
Dissection
Vasculitis
Buerger disease
HIV arteriopathy BOX 8-3
Radiation therapy
Collagen vascular diseases CLUES TO UNUSUAL
Extrinsic compression C AU S E S F O R P E R I P H E R A L
Vasospastic drugs (e.g., vasopressin, ergots, A RT E R I A L D I S E A S E
methysergide)
Raynaud disease Age "40 years
Popliteal artery disorders No risk factors for atherosclerosis or
Popliteal artery entrapment thromboembolism
Cystic adventitial disease Isolated, unilateral disease
Fibromuscular dysplasia Disease at unusual sites (e.g., common femoral
Iliac artery endofibrosis artery)
Atherosclerosis is a systemic disease. As such, it is aortoiliac and femoropopliteal segments are relatively
typically diffuse and bilateral. However, there is a spared. Medial calcification is distinctive of diabetic
clear predilection for clinically significant disease in arterial disease and chronic end-stage renal disease.
the distal aorta, common and external iliac arteries, Arterial obstructions tend to be more severe than in
distal SFA, and tibial arteries. The propensity for patients with atherosclerosis, and the collateral circu-
obstructions in the distal SFA as it passes through the lation often is less effective. For these reasons, non-
adductor canal is related to turbulent flow and altered healing ulcers, gangrene, and amputation are much
wall shear stress. These hemodynamic disturbances more common in this population.
result from changes in curvature and tortuosity of this Macroemboli usually are thrombi that originate from
mobile vessel along with compression on the vessel the heart. Less often, clot or plaque fragments break off
by the adductor magnus muscle and fascia at the ad- from aneurysms or atherosclerotic surfaces in the proxi-
ductor canal.17,18 Atherosclerotic plaques cause symp- mal arteries. Emboli usually lodge at branch points or
toms by impeding blood flow to the leg, inducing sites of underlying disease. Microemboli are composed of
thrombotic occlusion, or through embolization of clot platelet-fibrin deposits or cholesterol crystals arising
or plaque fragments. In CLI, obstructions are accom- from atherosclerotic plaques or aneurysms. These parti-
panied by abnormalities of skin microcirculation that cles may be released spontaneously or during operative
further exacerbate ischemia. manipulation or catheterization. Microemboli can lead
Diabetes is a strong risk factor for PAD. Extensive to blue toe syndrome or an acute cholesterol embolization
tibial and pedal artery disease is characteristic; the event (see Chapter 1).
194 II. AORTA AND PERIPHERAL ARTERIES
Clinical Features However, these disorders are not associated with a low
By definition, the diagnosis of chronic PAD requires ankle blood pressure (see later).
symptoms lasting more than 2 weeks. The severity of Ischemic skin changes may follow if the obstruc-
PAD often is graded according to the scale of Rutherford tions worsen or revascularization is not done. Ischemic
and Becker19 (Table 8-1). At least 50% of patients with ulcers often start with trivial skin injury, which is
PAD are asymptomatic or have atypical symptoms; in particularly dangerous in patients with diabetes with
some cases, limited physical activity prevents the onset peripheral neuropathy and altered sensation. The
of leg pain. Only 10% or so will ultimately develop CLI.14 toes are most affected, although arterial heel and mal-
Chronic PAD is unusual before age 40. Men are affected leolar ulcers do occur. Again, ischemic ulcers must
more frequently than women, as are nonwhite individu- be distinguished from traumatic, venous, or neuro-
als.14 Most patients have one or more risk factors for pathic lesions.14 Their appearance is sometimes
disease (see Box 8-2). These patients usually suffer from distinctive: located on the toes (or heel), dry with a
associated coronary artery disease, cerebrovascular dis- pale base, sharply marginated, and associated with
ease, or chronic renal insufficiency. PAD is an important severe pain. Ulcers about the malleoli or above the
marker of these conditions. ankle are usually venous in origin (see Chapter 15).
Intermittent claudication (IC) is the first symptom in Gangrene is the feared sequela of CLI. Amputation
some patients. IC is characterized by predictable and may then be necessary. Diabetic patients suffer a
reproducible calf, thigh, or buttock muscle pain or major amputation rate that is 5- to 10-fold greater
fatigue with exercise (especially walking on an incline) than the general PAD population.14
that is invariably relieved by rest. The pain does not Physical signs of long-standing PAD include de-
resolve with continued leg exercise. It rarely occurs in pendent rubor, leg coolness, delayed capillary refill
the foot. Unfortunately, a variety of unrelated conditions (#1 second), and trophic changes (e.g., hair loss over
are often confused with true claudication, including spi- the lower legs, thin shiny skin, nail thickening). With
nal stenosis, nerve root compression, arthritis, chronic advanced PAD, ulcers and gangrenous changes occur.
compartment syndrome, and venous claudication.14,20 The interventionalist should document the status of
Still, a careful history will usually distinguish among the bilateral femoral, popliteal, dorsal pedis, and
these entities. In a minority of afflicted patients, the posterior tibial artery pulses. The peripheral pulses
collateral circulation eventually becomes insufficient to are evaluated on a 2-point scale (2 $ full, 1 $ dimin-
prevent muscle ischemia at rest despite maximum ished, 0 $ absent). However, the pulse examination is
peripheral vasodilation. Chronic limb ischemia is present notoriously nonspecific for the degree and location
when symptoms of rest pain or ischemic skin changes of PAD. Nonpalpable peripheral pulses should be
are combined with an ankle-brachial index less than 0.50 examined with a Doppler probe. A venous signal may
(see later discussion). be pulsatile but vanishes with compression by the
Rest pain is usually localized to the (distal) foot, is transducer.
made worse with leg elevation (while sleeping), and is Patients with blue toe syndrome complain of relatively
relieved with dependency (e.g., dangling the limb off acute onset of painful, bluish-colored toes on one or both
the bed). The pain is often excruciating and unremitting feet.21,22 The symptoms often resolve but may recur and
and may require opiate analgesics for relief. Many of occasionally lead to tissue loss. The peripheral pulses
these patients also have peripheral neuropathic pain. often are intact.
Rest pain can be mistaken for isolated diabetic (or non-
diabetic) peripheral neuropathy, complex regional pain Natural History
syndrome, nerve root compression, or night cramps. Usually, the clinical progression of PAD is remarkably
slow. Only 25% of individuals with IC note worsening of
initial symptoms. In most patients, development of robust
collateral circulation, adaptation of leg muscles, and self-
TABLE 8-1 Rutherford-Becker Classification of Peripheral
imposed changes in activity or gait are responsible for the
Arterial Disease
oftentimes benign course of the condition. No more than
Grade Category Symptoms 10% of those diagnosed with PAD require revascular-
None
ization for CLI within 5 years of presentation.14
0 0
I 1 Mild claudication However, once CLI is present, the overall prognosis
I 2 Moderate claudication is dismal. Within 1 year, 25% of such patients will re-
I 3 Severe (lifestyle-limiting) claudication quire major amputation and another 25% will be dead.
II 4 Rest pain These disturbing figures reflect the nature of PAD: a
III 5 Nonhealing ulcers, focal gangrene
systemic vascular disease with a very high mortality
III 6 Major tissue loss
rate, largely from associated coronary artery disease or
8. PELVIC AND LOWER EXTREMITY ARTERIES 195
stroke (i.e., 30% at 5 years, 50% at 10 years).14,15 Almost every patients with suspicious symptoms and a normal study
patient who suffers from CLI is dead within a decade. at rest (see Fig. 8-6C). While walking on an inclined
treadmill, ankle and brachial pressure measurements
Noninvasive Testing are periodically recorded. A fall in ankle pressure is
Noninvasive vascular studies identify at-risk patients diagnostic of significant PAD.
with asymptomatic disease, confirm the diagnosis of Plethysmography (pulse volume recordings, PVR) utilizes
PAD in those with an equivocal history or physical find- changes in leg volume to reflect overall perfusion of the
ings, determine the severity and level of obstructions, limb.23 With mild or moderate PAD, digital or segmental
follow the progression of disease, and assess response to pulse volume tracings are dampened; with severe
endovascular and surgical therapy. The most commonly occlusive disease, the waveform is almost flat. This tech-
used tests are the ankle-brachial and toe indexes, seg- nique is particularly useful when segmental pressure
mental blood pressure measurements, and plethysmog- measurements are inaccurate, as in patients with non-
raphy (pulse-volume recording). compliant arteries.
The ankle-brachial index (ABI) is extremely sensitive
(95%) and specific (almost 100%) for the diagnosis of Imaging
PAD.14,23 It is an absolutely essential part of the evalua- A correct diagnosis of chronic lower extremity PAD can
tion of all patients with known or suspected PAD. The almost always be made through a combination of clini-
systolic blood pressure at the ankle is divided by the cal findings and noninvasive testing. Direct imaging is
systolic brachial arterial pressure to yield an index used almost solely to identify the nature, sites, and ex-
(Table 8-2). Rest pain usually requires an ABI less than tent of disease in patients whose symptoms warrant
0.5 or an absolute ankle pressure less than 50 mm Hg. endovascular or surgical treatment.
Ischemic ulcers can develop below a pressure of 50 to Atherosclerosis is typically diffuse, bilateral, and often
70 mm Hg. However, calcified or noncompressible strikingly symmetric. Patients with claudication usually
arteries (as found in patients with diabetes or chronic have single-level disease. With the notable exception of
renal failure) falsely elevate pressure measurements diabetic patients, patients with CLI almost always have
and can lead to underestimation of disease severity. In multilevel disease. Clinically relevant lesions include hemo-
this situation, toe pressure measurements are more useful. dynamically significant stenoses (as measured by pressure
The toe index is normally greater than 0.60. An abso- gradients or luminal diameter reduction of more than
lute toe pressure of greater than 30 mm Hg is generally 50%), diffuse long-segment atherosclerosis, thrombotic
required for wound healing. occlusions, and ulcerated or exophytic plaques. Plaques
Segmental blood pressures are obtained by sequen- may be characterized as focal or long, calcified or noncal-
tially inflating blood pressure cuffs around the upper cified, concentric or eccentric, and smooth or ulcerated.
thigh, lower thigh, calf, ankle, and toe. Several sets
of guidelines have been established to interpret these COLOR DOPPLER SONOGRAPHY
values.14,23 A drop of 20 to 30 mm Hg between levels (or Color Doppler (duplex) sonography is favored in
comparing legs at the same level) suggests a significant some laboratories for arterial mapping to depict and
stenosis or occlusion (Fig. 8-6A). Abnormal values at grade arterial stenoses and occlusions. The technique is
the upper thigh, lower thigh, calf, and ankle reflect sensitive (!80% to 90%) and quite specific (!95%).23,24
obstructions in the aortoiliac segments, SFA, femoro- The normal Doppler spectral pattern in these high-
popliteal segment, and tibial arteries, respectively (see resistance arteries is triphasic, with rapid forward flow
Fig. 8-6B). However, the correlation is not always pre- in systole followed by brief reversal of flow in early
cise; for example, proximal femoral artery disease diastole. Direct and indirect indicators of significant
can mimic aortoiliac disease. Segmental pressure mea- PAD are listed in Box 8-4.
surements after exercise can detect occult disease in
MAGNETIC RESONANCE ANGIOGRAPHY
Magnetic resonance (MR) angiography has revolution-
TABLE 8-2 Ankle-Brachial Index Classifications ized the evaluation of patients with PAD.25-28 When
properly performed, MR angiography provides images
Range Rutherford Grade Disease almost comparable in quality and form to conventional
"0.5 II or III Chronic limb ischemia catheter angiography with none of the associated risks
0.51 to 0.90 I Intermittent claudication (see Fig. 8-2). The sensitivity and specificity of state-
0.91 to 1.3 0 No significant PAD of-the-art MR angiography approaches or exceeds
#1.4 Noncompressible vessels, 95%26-30 (Figs. 8-7 and 8-8).
likely to have PAD
MR angiography is contraindicated in certain patients
PAD, peripheral artery disease. (e.g., those with pacemakers, intracranial clips, severe
196 II. AORTA AND PERIPHERAL ARTERIES
250
200
mm Hg
Right ankle
Left ankle
150
100
A B
FIGURE 8-7 Chronic aortoiliac occlusion on maximum intensity projection magnetic resonance angiogram of the pelvis (A) and thigh (B).
There is complete occlusion of the distal aorta, proximal right common iliac artery, and left common and external iliac arteries. The right external
iliac artery is diseased. Diffuse right superficial femoral artery (SFA) disease with a tight mid left SFA stenosis is present.
198 II. AORTA AND PERIPHERAL ARTERIES
A B
FIGURE 8-8 Acute occlusion of left deep femoral to below-knee popliteal artery bypass graft. History of a right nephrectomy and left renal
artery stent (A). Magnetic resonance angiogram shows a small infrarenal abdominal aortic aneurysm. The right renal artery is occluded (black arrow).
The proximal left renal artery is obscured by the stent. Proximal portions of both common iliac arteries are stenotic. A stenosis is evident in the left
common femoral artery (white arrow). B, The bypass graft is thrombosed. The right superficial femoral artery (SFA) is diffusely diseased, and the
left SFA is occluded.
A B
C D
FIGURE 8-9 Pelvic and extremity arteries at computed tomography angiography, including the pelvis (A and B), thigh (C), and calf (D). Diffuse
bilateral mid superficial femoral artery (SFA) disease is present. There are right distal popliteal and tibioperoneal trunk stenoses (white arrows).
Neither anterior tibial artery is opacified.
200 II. AORTA AND PERIPHERAL ARTERIES
B E
FIGURE 8-10 Correlation of computed tomography and catheter angiography for peripheral vascular disease. Frontal (A) and oblique
(B) shaded-surface display computed tomography reconstructions suggest complete right common iliac artery occlusion (black arrow), and
moderate left common iliac artery stenosis (white arrow). The former is confirmed on review of axial images (C). Note that significant
calcification partially obscures the occlusion on reformatted images. The findings were confirmed on a catheter angiogram in frontal
(D) and left posterior oblique (E) projections.
8. PELVIC AND LOWER EXTREMITY ARTERIES 201
A C
FIGURE 8-12 Provocation of a pressure gradient with vasodilators. A, This patient with left superficial femoral artery occlusion and
a moderate left external iliac artery stenosis (black arrow) is about to undergo infrainguinal bypass graft placement. B, No pressure gradient
was found between the aorta (A) and external iliac artery (I) with the initial pullback method. C, After intraarterial injection of 25 mg of
tolazoline, the repeat pullback pressure measurement showed a systolic gradient of 20 mm Hg that warranted treatment.
202 II. AORTA AND PERIPHERAL ARTERIES
A B
FIGURE 8-13 Eccentric atherosclerotic plaque. A, The left posterior oblique pelvic arteriogram shows right iliac stenosis and only
moderate disease of the left common iliac artery. Note the enlarged right lumbar artery indicating the significance of the right-sided disease.
B, The right posterior oblique projection shows the true severity of the left-sided disease (white arrow).
A B C
FIGURE 8-14 Right popliteal artery aneurysm. A, Initial right leg arteriogram shows complete occlusion of the upper popliteal artery.
An aneurysm was not initially suspected. B and C, After partial thrombolysis, the aneurysm becomes apparent.
8. PELVIC AND LOWER EXTREMITY ARTERIES 203
A B
A B
C D E
FIGURE 8-16 Embolism to both common femoral arteries (CFA) with severe left leg ischemia. A and B, Bilateral oblique pelvic arteriogra-
phy shows a near occlusive embolus to the right CFA (white arrow). The right deep femoral artery is blocked. A left CFA embolus is almost
completely obstructive and extends into the superficial and deep femoral arteries (black arrow). Blood flows from internal iliac artery collaterals
into deep femoral artery branches. C, Following initial treatment with 12 mg of t-PA, there is some lysis of clot. D and E, Following additional
thrombolytic therapy, the embolus is completely resolved with three vessel run-off in the calf.
8. PELVIC AND LOWER EXTREMITY ARTERIES 205
BOX 8-5
C O N S E RVA T I V E
MANAGEMENT OF
FIGURE 8-18 Puncture site neointimal hyperplasia at the origin P E R I P H E R A L A RT E R I A L
of the right superficial femoral artery after cardiac catheterization DISEASE
(arrow). Notably, no other vascular disease is seen.
(Supervised) exercise program
Smoking cessation
Dietary modifications (for weight and cholesterol
Category A disease: endovascular treatment
control)
preferred
Blood glucose control in diabetic patients (hemo-
Category B disease: endovascular treatment pre-
globin A1c " 7%)
ferred, unless an operation is planned for other PAD
Blood pressure control ("140/90 mm Hg,
Category C disease: surgical treatment preferred
"130/80 mm Hg if diabetic or renal failure, favor
unless patient is at high risk for operation
thiazides and ACE inhibitors)
Category D disease: surgical treatment is much
Statin therapy for dyslipidemia (to LDL cholesterol
preferred, endovascular therapy is inferior
"100 mg/dL)
The technical details of percutaneous arterial revascu- Daily antiplatelet therapy (aspirin or clopidogrel)
larization are considered in detail in Chapter 3. Selection for associated CAD and CVD rather than PAD
criteria, specific technical features, and outcomes at vari-
ous sites are discussed herein. Perhaps in no other area of ACE, angiotensin converting enzyme; CAD, coronary artery dis-
ease; CVD, cerebrovascular disease; LDL, low density lipoprotein.
interventional radiology are reports of the efficacy of a
procedure more disparate and confusing. Older radiologic
206 II. AORTA AND PERIPHERAL ARTERIES
A B C
D E
FIGURE 8-20 Radiation arteritis in a woman with a remote history of radiation therapy for cervical cancer and new right buttock claudication.
A and B, Shaded-surface display reformatted CT angiography shows entirely normal lower extremity arteries except left internal iliac artery (IIA)
occlusion and a moderate origin stenosis of the right internal iliac artery (arrow). Pelvic arteriogram (C) and selective right common iliac arterio-
gram in left anterior oblique projection (D) confirm these findings and show enlarged lumbar arteries providing collateral circulation into the pelvis.
E, Angioplasty of the right IIA gave a good technical result but did not improve symptoms, probably due to radiation-induced small vessel arteritis.
8. PELVIC AND LOWER EXTREMITY ARTERIES 207
Type A lesions
Unilateral or bilateral stenoses of CIA
Unilateral or bilateral single, short (3 cm) stenosis of EIA
Type B lesions
Short (3 cm) stenosis of infrarenal aorta
Unilateral CIA occlusion
Single or multiple stenosis totaling 3-10 cm involving
the EIA, not extending into the CFA
Unilateral EIA occlusion not involving the origins of
internal iliac or CFA
Type C lesions
Bilateral CIA occlusions
Bilateral EIA stenoses 3-10 cm long, not extending
into the CFA
Unilateral EIA stenosis extending into the CFA
Unilateral EIA occlusion that involves the origins of
internal iliac and/or CFA
Heavily calcified unilateral EIA occlusion with or
without involvement of origins of internal iliac and/or CFA
Type D lesions
Infrarenal aortoiliac occlusion
Diffuse disease involving the aorta and both iliac
arteries, requiring treatment
Diffuse multiple stenoses involving the unilateral
CIA, EIA, and CFA
Unilateral occlusions of both CIA and EIA
Bilateral occlusions of EIA
Iliac stenoses in patients with AAA requiring
treatment and not amenable to endograft
placement or other lesions requiring open
aortic or iliac surgery
A
FIGURE 8-22 A, TASC II classification of aortoiliac lesions. (Adapted from Norgren L, Hiatt WR, Dormandy JA, et al: Inter-society consensus for
the management of peripheral arterial disease [TASC II]. Eur J Vasc Endovasc Surg 2007;33:S1.)
8. PELVIC AND LOWER EXTREMITY ARTERIES 209
Type A lesions
Single stenosis 10 cm long
Single occlusion 5 cm long
Type B lesions
Multiple lesions (stenoses or occlusions), each 5 cm
Single stenosis or occlusion 15 cm, not involving the
infrageniculate popliteal artery
Single or multiple lesions in the absence of continuous
tibial vessels to improve inflow for a distal bypass
Heavily calcified occlusion 5 cm long
Single popliteal stenosis
Type C lesions
Multiple stenoses or occlusions totaling >15 cm with or
without heavy calcification
Recurrent stenoses or occlusions that need treatment
after two endovascular interventions
Type D lesions
Chronic total occlusions of CFA or SFA (>20 cm,
involving the popliteal artery)
Chronic total occlusion of popliteal artery and
proximal trifurcation vessels
B
FIGURE 8-22, contd B, TASC II classification of femoropopliteal lesions. (Adapted from Norgren L, Hiatt WR, Dormandy JA, et al: Inter-
society consensus for the management of peripheral arterial disease [TASC II]. Eur J Vasc Endovasc Surg 2007;33:S1.)
TABLE 8-3 Results of Transcatheter Therapy for Chronic Peripheral Arterial Disease
Technical
Site and Disease Therapy Success (%) 1-Yr Patency (%) 3-Yr Patency (%) 5-Yr Patency (%)
touching in the very distal aorta60,68 (see Fig. 8-24). primary patency rates of iliac artery stents (including
In this way, overhanging aortic disease is covered and occlusions) have been reported at 46% to 74%.70,71
a unilateral stent extending into the aortic lumen will Secondary patency rates at 3 years approach 90% to
not infringe on the contralateral common iliac artery. 95% with most devices. The most commonly reported
However, this common practice may be unnecessary if predictors of long-term durability are male gender,
the opposing iliac vessel is normal and the stent is abstinence from smoking, common iliac artery location,
deposited just up to the bifurcation.69 large arterial (stent) diameter, patent outflow arteries,
Table 8-3 summarizes the primary patency rates for
endovascular iliac artery treatment.* Eight- to 10-year *See references 14, 58-60, 64, 65, 70-73.
210 II. AORTA AND PERIPHERAL ARTERIES
TABLE 8-4 Ideal Conditions for Balloon Angioplasty of ILIAC ARTERY OCCLUSION (TASC TYPE B-D)
Lower Extremity Arteries
Endovascular therapy is an attractive alternative to sur-
Lesion Characteristics Patient Characteristics gery for some common or external iliac artery occlu-
sions. Balloon angioplasty alone is not sufficient; all of
Short Nondiabetic
these obstructions require a stent. It is also accepted
Concentric Milder degrees of ischemia
Noncalcified practice to skip thrombolysis or mechanical thrombec-
Solitary tomy and proceed directly to primary uncovered stent
Nonocclusive insertion once the obstruction is crossed.76
Large vessel An ipsilateral groin approach provides the most direct
Continuous in-line run-off
pathway to the obstruction. It is also preferable when
stents must be deployed up into the aorta. However, many
devices can be advanced from the opposite groin over the
bifurcation, through a guiding catheter or sheath, and then
short lesion length, and complete covering of the deployed in the main iliac artery trunks. Rarely, a brachial
diseased segment.14,70 For example, patency rates for artery approach is necessary. The occlusion is crossed with
common versus external iliac artery stent placement at a steerable hydrophilic guidewire. If the guidewire will
5 years in one study were 76% and 56%, respectively.74 only traverse the occlusion from the contralateral groin,
This response may be related to the smaller size of the tip can be snared from the ipsilateral CFA and pulled
the vessel and the fact that hip flexion causes arterial through the sheath. An angiographic catheter is then
angulation in this region (not just around the CFA as placed in a retrograde direction for stent placement. Stents
commonly believed).75 may be inserted even when guidewire passage is partially
Complications (most of which are minor) occur in subintimal, as long as the wire reenters the lumen before
about 10% of cases and include puncture site injury or reaching the aorta. Stents are deposited along the entire
hematoma, acute stent thrombosis, distal embolization, length of the occlusion, incorporating adjacent segments
stent dislodgment, pseudoaneurysm formation, and ves- of significant atherosclerotic disease. Placement of stents
sel rupture. well into the CFA is controversial (see later discussion).
8. PELVIC AND LOWER EXTREMITY ARTERIES 211
A B
C D
E
212 II. AORTA AND PERIPHERAL ARTERIES
A B
C D
FIGURE 8-26 Superficial femoral artery angioplasty and stent placement. A, Arteriogram reveals an ideal lesion for angioplasty. B, Although
the balloon inflated completely, follow-up angiogram showed elastic recoil (not shown). C, Nitinol SMART stent inserted to limit remodeling.
D, Widely patent artery afterwards.
214 II. AORTA AND PERIPHERAL ARTERIES
A B C
FIGURE 8-27 Superficial femoral artery (SFA) balloon angioplasty. A, Right leg arteriogram shows a critical mid-SFA stenosis (arrow).
B, A microwire and catheter were used to cross the site. The catheter is occlusive in the lesion. C, Following angioplasty with a 5-mm & 2-cm
balloon, there is marked improvement in patency and collateral circulation is diminished.
for use of these devices in complex or longer TABLE 8-5 Endovascular Options for Femoropopliteal
femoropopliteal lesions (e.g., #5 to 10 cm).115-118 Arterial Obstructions
On the other hand, stents composed of other mate- Lesion Options
rials or of the balloon-expandable variety should be
avoided. The advantages of nitinol include greater Short, simple FP stenosis PTA
Resistant stenosis Cutting balloon
radial force and flexibility, minimal plastic defor-
Elastic recoil stenosis Bare nitinol stent
mity, and more predictable lesion coverage due Post PTA dissection Bare nitinol stent
to minimal shortening at deployment. Two vexing Complex #5-10 cm FP Bare nitinol stent
and persistent problems with some current devices stenosis
are in-stent restenosis and stent fracture, both of Multiple FP stenoses PTA or bare nitinol stent
Angioplasty failure Bare nitinol stent
which can reduce overall patency.112,119
Short FP occlusion Bare nitinol stent (or ePTFE stent
Drug-eluting bare stents (DES) are currently the graft)
subject of intense research for infrainguinal revas- Long segment FP occlusion ePTFE stent graft or subintimal
cularization. They have shown dramatic results in recanalization
the coronary circulation, where clinically significant
ePTFE, expanded polytetrafluoroethylene; FP, femoropopliteal; PTA, conventional
restenosis has been markedly reduced. A polymer balloon angioplasty.
matrix is bonded to the bare metal stent. The matrix
affords controlled release of an agent chosen to
retard the process of neointimal hyperplasia. For longer femoropopliteal occlusions in patients who are
The principal drugs under study are sirolimus not candidates for surgical bypass (due to lack of vein
and everolimus (lipophilic macrocyclic drugs with conduit or operative risks), recanalization of the entire
immunosuppressive and antibiotic activity) and occluded vessel with ePTFE-covered stents is perhaps the
paclitaxel (a lipophilic diterpenoid that inhibits best choice (Fig. 8-30).
cell function by microtubule stabilization, thus Subintimal angioplasty is advocated by some experts for
preventing smooth muscle cell proliferation and treating long-segment femoropopliteal artery occlu-
migration).120 To date, results of DES in femoro- sions.128-132 Again, this technique is usually reserved for
popliteal artery obstructions have been mixed. patients with high operative risk or no suitable vein
The SIROCCO (sirolimus-based) and STRIDES for bypass. A distal target vessel that will ultimately pro-
(everolimus-based) trials did not support use vide in-line run-off to the foot must be present.
of these devices.121,122 However, preliminary Access is gained through the contralateral or ipsilateral
unpublished work from the Zilver PTX (paclitaxel- CFA, or retrograde from the popliteal artery. The optimal
based) trial is quite promising.123 entry (diseased) and exit (nondiseased) points are deter-
ePTFE covered stent grafts show great promise for mined. With an angled angiographic catheter wedged
femoropopliteal obstructions that do not respond to at the diseased upper (or lower) arterial segment, a
balloon angioplasty.124,125 A randomized, multicenter 0.035-inch angled hydrophilic guidewire is directed
trial conducted more than 10 years ago (largely in subintimally. A small loop is formed with the wire; a
claudicants) found significantly improved target reinforced, hydrophilic catheter is then advanced to the
vessel patency and limb ischemia status in the loop, and the entire unit is run down (or up) the subinti-
Viabahn stent graft group compared with angio- mal space until the planned exit site is reached. The lumen
plasty alone, particularly for lesions greater than is then reentered with the wire tip. Alternatively, the Out-
3 to 13 cm in length.124 The ongoing VIASTAR trial back reentry catheter accomplishes the same thing.133-135
will compare a bare nitinol stent with the Viabahn The entire channel is widened with an angioplasty bal-
Propaten (heparin-bonded coating) platform. Most loon; stents are used selectively as needed. The reported
patients receive aspirin or clopidogrel before and technical success (in experienced hands) is 80% to 90%,
for at least several months after covered stent and 1-year limb salvage rates are 75% to 90%. In one
placement.126,127 report, these salvage rates persisted at 3 years.136
Table 8-5 summarizes current recommendations for There are two major risks from subintimal angio-
treatment of femoropopliteal lesions. Methods must be plasty: bleeding and worsening of ischemia. To prevent
tailored to the availability and local advisory board bleeding in case transmural perforation occurs, full
approval of the various devices. anticoagulation is delayed until the channel is created.
Rarely, coil embolization of the tract is necessary. In
FEMOROPOPLITEAL ARTERY OCCLUSION addition, worsening of ischemia may result from occlu-
(TASC C AND D LESIONS) sion of important collateral branches if the procedure is
At present, three endovascular options are considered. not successful.
(see Table 8-5). For short ("3 to 5 cm) total femoropopliteal Mechanical revascularization devices (e.g., Amplatz
occlusions, bare nitinol stents are appropriate (Fig. 8-29). thrombectomy catheter) have excellent technical success
216 II. AORTA AND PERIPHERAL ARTERIES
A B C
D E
FIGURE 8-29 Angioplasty and stent placement for a left superficial femoral artery (SFA) occlusion. A, Distal SFA occlusion. Note that the
actual length of the obstruction (between arrows) is relatively short because of backfilling from the collateral circulation. B, After 5-mm balloon
angioplasty, a long dissection flap is seen. C, Embolic occlusion of the tibioperoneal trunk and anterior tibial artery (arrow) has occurred.
D, After angioplasty, flow in the peroneal artery has been reestablished. E, Following placement of two overlapping SMART Control stents,
the SFA is widely patent. (Courtesy of David Lopresti, MD, San Diego, Calif.)
8. PELVIC AND LOWER EXTREMITY ARTERIES 217
D E F G
in some series, but long-term patency and limb salvage amputation site or to avoid amputation altogether.137
rates have not been substantiated. However, tibial recanalization is much less effective
when in-line run-off (continuous flow to the pedal
TIBIAL ARTERY OBSTRUCTION arch) is not reestablished or when heroic procedures
Infrapopliteal endovascular interventions are almost are performed on patients with severe, widespread in-
always performed for limb salvage (Fig. 8-31). Al- frapopliteal disease because they are poor surgical
though durability of angioplasty is inferior to distal candidates.
vein bypass grafts, even short-term patency may Endovascular options include conventional balloon
be sufficient to allow healing of an ischemic ulcer or angioplasty, bare stent placement, or drug-eluting
218 II. AORTA AND PERIPHERAL ARTERIES
A B
stent insertion. The latter measures are clearly appro- For arterial rupture, the balloon is advanced across the
priate for angioplasty failures.138,139 Limited evidence torn artery and reinflated. Some ruptures close with this
to date supports DES over bare stents for this applica- maneuver. If not, placement of a covered stent is usually
tion.139,140 Technical success can be anticipated for most effective. Otherwise, surgical repair may be needed if the
stenotic lesions (see Table 8-3). Outcomes are better for vessel continues to bleed.
stenoses than occlusions (patency at 1 year, 68% vs. 48%,
respectively).141 Liberal use of heparin is important to Surgical Therapy
maintain vessel patency after angioplasty. Intraproce- For aortoiliac occlusions, surgical options include an AFB
dural intraarterial vasodilators may prevent or limit graft, extraanatomic graft, or (rarely) endarterectomy.142
vessel spasm. When the external iliac artery is patent, the distal anasto-
mosis is made in an end-to-side fashion to the CFA to
COMPLICATIONS maintain perfusion to the pelvis and left colon (Fig. 8-33).
Although most angioplasty and stent procedures pro- Extraanatomic conduits include axillobifemoral, axillo-
ceed without incident, several problems can arise (see femoral, and femorofemoral grafts (Fig. 8-34). These grafts are
Chapter 3). preferred in patients with unilateral iliac disease, high
Vasospasm is most frequently encountered during surgical risk, severe scarring from multiple prior vascular
angioplasty below the knee (Fig. 8-32). Spasm may be procedures, abdominal or groin infections, or chronic
largely prevented by giving a vasodilator (e.g., nitroglyc- occlusion of one limb of an AFB. The 5-year patency of an
erin 100 to 200 !g) immediately before dilation. If severe AFB placed for occlusive disease is 85% to 95%.142 Compli-
spasm occurs, more heparin is administered immediately cations of bypass grafts are discussed in a later section.
(as needed) to prevent occlusion. Spasm usually resolves Infrainguinal arterial occlusions not suitable for
with additional intraarterial vasodilator and time. endovascular therapy are treated with a bypass graft.
Repeat angioplasty is performed for acute thrombosis The large BASIL study confirmed the conventional
immediately after angioplasty. If the occlusion is long, a wisdom that late outcomes (#2 years) were better
brief trial of thrombolytic therapy followed by repeat with infrainguinal surgical bypass than angioplasty as
angioplasty and stent placement often is successful. first treatment, although results with prosthetic graft
8. PELVIC AND LOWER EXTREMITY ARTERIES 219
A B C
FIGURE 8-32 Vasospasm after balloon angioplasty. A, Tight stenoses of the popliteal artery are just beyond a bypass graft anastomosis
(arrows). B, Severe vasospasm occurred after initial angioplasty with a 4-mm balloon. C, The vasospasm resolved with additional heparin,
intraarterial nitroglycerin (200 !g), and time.
material were poor.143,144 The indications for an above- expected with distal pedal bypass procedures if patients
knee synthetic (PTFE) bypass graft are vanishing. Two are properly selected, with 3-year patency and limb
other randomized studies found that patients with salvage rates of about 60% and 90%, respectively.150-152
SFA occlusive disease had comparable benefit from
this form of bypass and ePTFE/nitinol self-expanding Acute Lower Extremity Ischemia
stent placement.145,146 Thus all above-knee femoropop- (Online Cases 28, 43, and 99)
liteal and distal below-knee femoropopliteal, tibial,
and pedal grafts should be constructed with vein. If Etiology
suitable vein is not available, an endovascular approach The most frequent reasons for acute lower extremity
is generally favored. ischemia are embolization, thrombosis of diseased native
Reversed saphenous vein grafts are created by ligating all arteries, and occlusion of bypass grafts14,153 (Box 8-6).
major tributaries of the vessel, harvesting the graft, and Less common causes include trauma and peripheral
then reversing it so that blood can flow through the valves. aneurysm thrombosis or distal embolization. The sever-
In situ saphenous vein grafts are constructed by ligating ity of symptoms is largely determined by the maturity
all main tributaries of the dissected vein, anastomosing of the collateral circulation. If blood flow is markedly
the proximal and distal ends to the appropriate arteries, compromised and revascularization is delayed, the result
and destroying the valves with an endoluminal valvulo- may be muscle/skin necrosis or nerve injury. Acute limb
tome to permit antegrade flow. When the ipsilateral ischemia is a very serious condition. Even in contempo-
saphenous vein is not suitable, the choices are among rary reports, the mortality rate approaches 20%.14
short or accessory saphenous veins, the contralateral Macroemboli typically arise from the heart in patients
great saphenous vein, or superficial upper arm vein.147 with some form of cardiac disease. Less often, clot or
A critical step in preoperative planning is to identify a large plaque fragments migrate from a proximal artery.154
target vessel for distal bypass. Ideally, the selected tibial Immediately after the embolic event, downstream arteries
artery has continuous in-line run-off to the pedal arch. constrict. Clot then propagates proximally or distally to
More than 70% to 80% of in situ lower extremity saphe- the next large collateral branch(es). Microemboli are
nous vein grafts are patent 5 years after placement.148 minute particles composed of cholesterol crystals, fibrin-
Outcomes are less favorable with prosthetic material and platelet deposits, or cellular thrombi that break off from
poor with umbilical vein conduit.149 Good results are proximal ulcerated plaques or aneurysms155,156 (see
220 II. AORTA AND PERIPHERAL ARTERIES
Chapter 1). The source usually is the aorta or iliac arter- enough for collateral channels to develop, the patient
ies.157,158 Cholesterol embolization syndrome is an acute, may present with chronic symptoms rather than sudden
life-threatening event usually precipitated by catheter- onset of ischemia. In situ thrombosis without underlying
ization or aortic manipulation. Blue toe syndrome is a more disease virtually always occurs in patients with a throm-
subacute or chronic condition resulting from spontane- bophilic state (see Chapter 1 and Boxes 1-4 and 1-5).
ous embolization of microemboli. Recurrent embolic
showers are the rule, resulting in necrosis and tissue loss Clinical Features
in about 60% of cases. By convention, acute lower extremity ischemia implies
In a native artery or a bypass graft, acute thrombotic symptoms of less than 2 weeks duration.14 The physician
occlusion usually is superimposed on underlying can usually elicit a history of cardiac disease, atrial dys-
disease. If blood flow has been compromised long rhythmias, claudication, or prior bypass graft placement.
A B
C
8. PELVIC AND LOWER EXTREMITY ARTERIES 221
The classic 5 Ps of a cold leg from acute ischemia are arteriogram is done from the contralateral groin
pain, pulselessness, pallor, paresthesia, and paralysis. (Fig. 8-35). However, if recent imaging studies docu-
The pulse examination helps determine the level of ment normal aortoiliac inflow, direct antegrade CFA
obstruction. The grade of acute ischemia is determined puncture on the affected side can simplify thrombolysis
by physical examination and Doppler signal in the foot and subsequent angioplasty, as long as there is suffi-
(Table 8-6). Classification is critical because it guides the cient room to enter the CFA below the inguinal ligament
mode of therapy. and select the graft or artery (see Chapter 3).
The dramatic presentation of cholesterol emboliza- Embolism may be impossible to differentiate from
tion syndrome is the abrupt onset of a painful, white, acute thrombosis, although certain angiographic fea-
marbled extremity (livido reticularis), often accompa- tures are characteristic (Fig. 8-36 and see Fig. 1-12; see
nied by acute renal failure or mesenteric ischemia. also Box 1-8). Most macroemboli lodge in the femoral or
popliteal artery. Total occlusion can hide an unusual
cause for thrombosis, such as a popliteal artery aneu-
Imaging
rysm (see Fig. 8-14). Rarely, the thoracic aorta is a source
COMPUTED TOMOGRAPHY AND MAGNETIC of lower extremity emboli (see Fig. 8-36). In situ throm-
RESONANCE ANGIOGRAPHY bosis often appears as wormlike filling defects that
For some patients, immediate surgery without preoper- simulate emboli (see Fig. 1-11).
ative imaging is appropriate. If the degree of ischemia is In patients with microembolization syndromes,
relatively mild and intervention is contemplated, CT or proximal atherosclerotic disease (particularly shaggy,
MR angiography can be used to confirm the diagnosis ulcerated plaques) or aneurysms usually are detected
and tailor the operative strategy. in the abdominal aorta, iliac arteries, or SFA (Fig. 8-37).
It is sometimes impossible to determine which of
CATHETER ANGIOGRAPHY multiple lesions is responsible for embolic events.
The majority of patients with acute lower extremity Although a continuous channel usually exists between
ischemia will benefit from initial endovascular therapy. the presumed source and the feet, microemboli can
Therefore, catheter arteriography should be the first pass through collateral beds around major arterial
study after presentation. Traditionally, the diagnostic obstructions.
222 II. AORTA AND PERIPHERAL ARTERIES
A B
TECHNIQUE
The options for endovascular removal of acute lower
ultrasound confirms or excludes the diagnosis. extremity arterial thrombus include the following:
Many experts support catheter-directed throm-
Catheter-directed fibrinolytic drug infusion
bolysis before definitive aneurysm treatment14
Pharmacomechanical thrombolysis (e.g., Trellis
(see later section).
device)
Endovascular Therapy Ultrasound-enhanced catheter-directed thrombol-
ysis179
Enzymatic thrombolysis, mechanical thrombectomy, or
Mechanical thrombectomy (e.g., AngioJet device)
thromboaspiration are used to manage many acute lower
Aspiration thrombectomy
extremity arterial occlusions165-174 (see Chapter 3). Clot
dissolves easily because it is relatively fresh; fibrinolytic The details and relative merits of these various methods
agents lyse small vessel thrombus that is inaccessible to are considered in Chapter 3. Strict adherence to recent
*See references 166-169, 174, 180-182. *See references 153, 170, 171, 195-197.
8. PELVIC AND LOWER EXTREMITY ARTERIES 225
A B C
D E
FIGURE 8-36 Thrombolysis of a left popliteal artery embolus. A through C, Left leg arteriography shows a filling defect in the above-knee
popliteal artery (black arrow). The collateral circulation is very immature. The proximal femoral arteries are entirely normal. There is distal reconsti-
tution of the tibioperoneal trunk (white arrow). D, A multiside hole infusion catheter now spans the occlusion. E, After overnight thrombolysis with
tissue plasminogen activator at 1 mg/hr, the thrombus is completely lysed with no underlying disease. F, Later, contrast-enhanced computed
tomography scan shows the probable culprit thrombus in the descending thoracic aorta (white arrow).
226 II. AORTA AND PERIPHERAL ARTERIES
A B
FIGURE 8-37 Iliac artery stent placement for left-sided blue toe syndrome. A, A complex, ulcerated plaque is detected in the distal left
external iliac artery (arrow). B, Primary stent placement was done to remodel and cover the plaque to prevent recurrent microembolization.
presence of organized clot, inadequate anticoagulation, a restoration of blood flow. The diagnosis is suggested
thrombophilic state, and poor run-off. by pain, sensory deficits, and swelling. Fasciotomy is
Three randomized clinical trials (STILES, TOPAS, usually necessary when the intracompartment pressure
University of Rochester) have substantiated the equiva- exceeds 20 mm Hg.
lence of catheter-directed thrombolysis and surgery in Reperfusion syndrome is a consequence of massive
patients with acute lower extremity arterial ischemia rhabdomyolysis, which is manifested by a spike in serum
with respect to limb salvage and mortality.165,175-177,199 In creatine kinase (#5000 units/L), myoglobinuria (with
patients suffering from microembolization syndromes, tea-colored urine), and acute renal failure.14 Standard
PTA and stents are sometimes effective in remodelling, treatment is vigorous IV hydration and alkalinization of
removing, or covering the embolic surface and prevent- the urine.
ing recurrent showering of particles200 (see Fig. 8-37).
Surgical Therapy
COMPLICATIONS Operative revascularization entails bypass proce-
The most important adverse events from lower ex- dures almost identical to those used for chronic limb
tremity thrombolytic therapy are outlined in Table 3-6. ischemia (see previous discussion). For acute embolic
Major complications are relatively frequent in some occlusions, Fogarty balloon thromboembolectomy
series. Causes of bleeding are multifactorial and or intraoperative fibrinolytic infusion are used. Ulti-
include a systemic lytic state from fibrinogen deple- mately, the offending source of emboli must be
tion, lysis of hemostatic plugs (e.g., in the brain) by removed, remodeled, or excluded by endovascular or
fibrin-specific agents, effects of anticoagulants or anti- operative means.
platelet agents, and patient-related factors. Other
problems include pericatheter thrombosis, reperfusion Arterial Bypass Graft Failure
or compartment syndrome, drug reaction, and vessel (Online Cases 43 and 97)
or graft extravasation.
About 15% of patients require fasciotomy for com- Etiology and Clinical Features
partment syndrome following revascularization of an Immediate complications of an AFB graft include occlu-
ischemic limb.14 This disorder reflects increased capil- sion, bleeding, colonic ischemia, and spinal cord ischemia.
lary permeability and fluid accumulation within the Late complications include infection, pseudoaneurysm
anterior (and less often posterior) fascial space following formation, partial or complete thrombosis, and aortoenteric
8. PELVIC AND LOWER EXTREMITY ARTERIES 227
A B
C D
FIGURE 8-38 Iliac artery thrombolysis for acute ischemic symptoms. A, Right posterior oblique pelvic angiogram shows complete
occlusion of a graft (between arrows) from the right external iliac artery to the deep femoral artery. B, A guiding sheath was placed over the
aortic bifurcation and the occlusion traversed with an angled hydrophilic guidewire. A pulse-spray catheter with multiple side slits spans
the lesion. C, After 35 minutes of periodic injection of tissue plasminogen activator to a dose of 4 mg, there is substantial lysis. D, Following
additional overnight infusion of the drug at 0.5 mg/hr, the graft is widely patent.
fistula (see Fig. 7-13). Early graft thrombosis often is neointimal hyperplasia, progression of atherosclerosis,
the result of an operative error. Late graft thrombosis is and poor run-off. About half of the obstructions de-
caused by neointimal hyperplasia at graft anastomoses, velop within the graft, and the remainder occur at the
progressive atherosclerosis, pseudoaneurysm formation, anastomoses or within native arteries.201
or infection. Most patients with acute graft thrombosis present
Early or subacute infrainguinal bypass graft failure with sudden onset of ischemia (see earlier). However,
has several causes (Box 8-7). The major reasons for de- less than 50% of individuals with graft dysfunction and
layed infrainguinal graft failure are graft stenosis from impending failure are symptomatic.
228 II. AORTA AND PERIPHERAL ARTERIES
C D
Surgical Therapy
Failing grafts are repaired with a patch graft or graft
extension. Retained valves are obliterated with an endo-
luminal valvulotome. Clotted grafts require surgical
thrombectomy and revision or complete graft replace-
ment. With infrainguinal conduits, the 2-year patency
rate for the former approach is less than 40%.211
A B C
FIGURE 8-41 Stenosis of an in situ saphenous vein bypass graft in an asymptomatic patient. A, The sonogram detected overall diminished
velocities (13 to 28 cm/sec) but a markedly increased velocity (512 cm/sec) in the middle thigh. B, A critical intragraft stenosis was discovered
at catheter angiography (arrow). C, It was treated successfully with a 4-mm balloon.
Clinical Features
Pelvic and lower extremity degenerative aneurysms are
FIGURE 8-42 Long-segment fibrosis of a right saphenous vein very much a disease of men.216,217 Many patients with
infrainguinal bypass graft. iliac artery aneurysms are asymptomatic. In particular,
8. PELVIC AND LOWER EXTREMITY ARTERIES 231
A B
Imaging
CROSS-SECTIONAL TECHNIQUES
For aneurysm detection and surveillance, MR or CT
imaging is used for the iliac arteries and color Doppler
sonography for the infrainguinal arteries.227 Sonogra-
phy is essentially 100% accurate in the diagnosis of
postcatheterization pseudoaneurysms. These lesions
are characterized by swirling color flow in the aneu-
rysm sac and to-and-fro flow at the aneurysm neck
(see Figs. 3-10 and 3-12). On MR or CT angiography, a
pelvic or peripheral aneurysm may display intimal
calcification, fusiform widening of the artery, and mu-
ral thrombus228 (Figs. 8-45 through 8-48). Popliteal
artery aneurysms usually spare the distal segment of
FIGURE 8-44 Aortobifemoral bypass graft with pseudoaneurysm of
left distal anastomosis (arrow) and complete occlusion of right limb.
the artery.
CATHETER ANGIOGRAPHY
internal iliac artery aneurysms often are silent until they Degenerative aneurysms are typically fusiform and may
rupture.223,226 Warning symptoms are related to com- be solitary or multiple. Aneurysms that are saccular, ec-
pression of adjacent structures or (rarely) fistulization centric, or atypical in location should raise the suspicion
with a pelvic organ. Up to one third of popliteal artery of an unusual cause, such as infection or trauma (see
aneurysms are unsuspected at the time of diagnosis.220 Fig. 8-48). Aneurysms can be missed at angiography
232 II. AORTA AND PERIPHERAL ARTERIES
C AU S E S O F P E LV I C A N D Endovascular Therapy
LOWER EXTREMITY When anatomically feasible, common iliac artery aneu-
A N E U RY S M S rysms (contained or ruptured) are usually repaired by
endovascular means with stent grafts. Preemptive
True Aneurysms embolization of the ipsilateral internal iliac artery may
Degenerative be necessary to avoid a type II endoleak (see Chapter 7)
Infectious (mycotic) after device deployment. Published results (including
Noninflammatory vasculopathy patency rates and subsequent rupture rates) have been
Marfan syndrome excellent.217,229-232
Ehlers-Danlos syndrome The rationale for repair of popliteal artery aneu-
Human immunodeficiency virus arteriopathy rysms is prevention of ischemia and limb loss from
Vasculitis aneurysm thrombosis or distal embolization. Elective
Behet disease treatment of asymptomatic lesions is usually recom-
Polyarteritis nodosa mended when the aneurysm is greater than 2 cm or
Congenital mural thrombus is detected.233-235 However, the pres-
ence of symptomatic nerve or vein compression man-
False Aneurysms dates operation. Stent grafts have become very popular
among interventionalists in this setting, especially in
Traumatic individuals at high risk for operation or who lack
Iatrogenic suitable vein for bypass. The ePTFE-nitinol Viabahn
Accidental device is favored by many operators. Deployment is
Anastomotic usually done with an antegrade femoral artery punc-
Infectious ture. The graft is oversized to no more than 10% to 15%
Erosive (e.g., extrinsic compression by osteophytes) of the nominal diameter of the vessel. Stents should be
inserted with knowledge of the vascular flexion point
A B
FIGURE 8-45 Ruptured, isolated left internal iliac artery aneurysm. A and B, Axial and reformatted coronal computed tomography images
show aneurysmal enlargement of the calcified left internal iliac artery (black arrows). A pseudoaneurysm has been produced from contained rup-
ture. Surrounding low-density fluid suggests prior leak (white arrows). A right iliac artery aneurysm is also noted (most rightward black arrow).
8. PELVIC AND LOWER EXTREMITY ARTERIES 233
C D
as determined at fluoroscopy. Proximal and distal difference in primary or secondary patency rates at
landing zones of at least 2 cm are necessary.234 Tandem 3 years for open and endovascular treatment.219,236
grafts should have at least 2 cm overlap in case of In patients with acute ischemia from popliteal artery
delayed component separation. Aspirin and clopido- aneurysm thrombosis or distal embolization, throm-
grel are prescribed for at least 3 months afterward to bolysis before definitive repair is now standard of
optimize patency. Patients are followed with periodic care161,163,234,237 (see Fig. 8-14).
imaging for late complications including graft throm- Internal iliac artery aneurysms are notorious for
bosis and endoleak (types II, I or III; see Chapter 7). completely unexpected rupture; elective repair is indi-
A recent metaanalysis of the existing literature and cated in most cases. They can be obliterated with com-
one randomized controlled trial showed no significant plete internal iliac artery embolization (see Fig. 8-45) or
234 II. AORTA AND PERIPHERAL ARTERIES
A B
C D E
FIGURE 8-46 Popliteal artery (PA) aneurysm. A and B, Axial and reformatted shaded-surface display computed tomography images show a
large, bipartite, above-knee, right PA aneurysm with wall calcification and mural thrombus. A left-sided aneurysm had been previously repaired
with a prosthetic bypass graft (arrow). C and D, Right leg angiography shows the tandem degenerative PA aneurysms with diffuse arteriomegaly
in the intervening segments. E, The aneurysms were treated by endovascular Viabahn stent graft placement, which has restored a normal lumen.
8. PELVIC AND LOWER EXTREMITY ARTERIES 235
B
236 II. AORTA AND PERIPHERAL ARTERIES
distal occlusion of the vessel followed by placement of first. Then the following sources of bleeding should
a covered stent over its origin.238,239 Distal embolization be considered:
is necessary to prevent aneurysm backfilling through
Bilateral internal iliac arteries and branches.
pelvic collaterals. Treatment of postcatheterization
Identification of one bleeding vessel does
pseudoaneurysms240-242 is described in Chapter 3.
not end the search for other lesions
Surgical Therapy Bilateral external iliac arteries and branches246
(e.g., inferior epigastric artery, anomalous
Iliac and CFA aneurysms are excluded with a bypass
origin of obturator artery; Fig. 8-49 and
graft. Postcatheterization femoral artery pseudoaneu-
see Fig. 8-4)
rysms are operated only if percutaneous thrombin injec-
Lumbar arteries247 (Fig. 8-50)
tion or ultrasound-guided neck compression fails and
Visceral arteries if there is any suspicion of
the aneurysm continues to expand. Open PAA repair
hemorrhage from a solid organ
involves saphenous vein bypass grafting with proximal
and distal aneurysm ligation.161-164,237 The mean 5-year Arterial hemorrhage is marked by discrete and focal,
patency rate is about 72%.219 or multiple punctate sites of contrast extravasation (see
Fig. 1-37). Additional findings include abrupt vessel
Pelvic Trauma (Online Cases 54 and 80) occlusion and severe tapering from vasospasm. Care
must be taken not to mistake bowel activity, hypervas-
Etiology and Clinical Features cularity, or road dirt for a bleeding site. The most
Because the branches of the internal iliac artery commonly injured vessels are the superior gluteal and
run close to the bony and ligamentous structures of internal pudendal arteries.
the pelvis, they are frequently injured during severe
blunt pelvic trauma from motor vehicle crashes, falls Treatment
from a height, and crush accidents. The mechanism Management begins with immediate resuscitation
of injury in the subgroup with persistent arterial followed by clinical and imaging assessment for associ-
bleeding often is severe anteroposterior compres- ated injuries. Venous and minor arterial bleeding often
sion (with diastasis of the symphysis pubis, pubic stop with external compressive fixation of the pelvis done
rami fractures, and sacroiliac joint disruption) or in a variety of ways. In isolated pelvic trauma, surgery is
lateral compression (with sacral and pubic rami generally avoided, because it is almost impossible to find
fractures).243,244 the bleeding vessels at operation and because exploration
Most patients with pelvic arterial hemorrhage are releases the tamponading effect of the hematoma below
hypotensive, and some have extensive multiorgan in- the pelvic peritoneum. Angiography with intent to embo-
jury. The initial decision to opt for conservative manage- lize is indicated for the following244,248:
ment, angiographic evaluation, or operation is often a
Hemodynamically unstable patients with negative
difficult one.
FAST or presence of pelvic hematoma on CT
Hemodynamically stable patient with active
Imaging bleeding on pelvic CT scan and no evidence of
CROSS-SECTIONAL IMAGING hollow viscus injury that would demand operation
Identification of pelvic hematoma at laparotomy
In most trauma centers, focused abdominal sonography
with persistent hypotension
in trauma (FAST) has replaced diagnostic peritoneal la-
Elderly patients or long duration of hypotension
vage (DPL) to identify abdominal bleeding that requires
whether stable or unstable (controversial)249
immediate operation. CT scanning is also extremely
valuable in this setting.245 It delineates pelvic fractures,
associated hematomas, active arterial or venous bleed- ENDOVASCULAR THERAPY
ing, and any associated internal organ injury. However, Embolization is the definitive therapy for traumatic
the place of CT in initial pelvic trauma management is pelvic arterial hemorrhage (see Figs. 8-49 and 8-50). If
still debated. the patient is exsanguinating and massive extravasation
is seen, bleeding must be stopped with alacrity by
CATHETER ANGIOGRAPHY rapidly depositing stainless steel coils, Gelfoam, or both
Evaluation starts with nonselective arteriography of in the proximal internal iliac artery. In most situations,
the entire pelvis and femoral regions. This step pro- however, there is time for selective embolization of the
vides a road map for further catheterization and damaged arteries. If multiple bleeding sites are found,
identifies massive bleeding that must be addressed scatter (shower) embolization with small Gelfoam
8. PELVIC AND LOWER EXTREMITY ARTERIES 237
A B
C D
E F
FIGURE 8-49 Arterial bleeding from pelvic injury due to a motor vehicle collision. A and B, The initial pelvic arteriogram did not show bleed-
ing. C, Left internal iliac arteriography shows probable extravasation (white arrow) but it did not appear to arise from that vessel. A focal density in
the left medial pelvis (black arrow) proved to be artifactual. D and E, Left external iliac arteriography identifies the external pudendal artery as the
likely culprit (arrow), which was proven with coaxial microcatheterization of that vessel. F, The vessel was embolized with microcoils and a single
small Gelfoam piece.
238 II. AORTA AND PERIPHERAL ARTERIES
A B
pieces often is appropriate (see Chapter 3). Some inter- after pelvic fractures) is probably related to the injury
ventionalists embolize truncated or narrowed arteries itself rather than embolization.252
that are not actively bleeding on the grounds that hem-
orrhage may have come or may resume from these in- Lower Extremity Trauma (Online Case 5)
jured vessels. The vascular beds that should be examined
are outlined previously. After embolotherapy is complete, Etiology and Clinical Features
it is wise to reinject both internal iliac arteries to confirm Lower extremity arteries are subject to injury from
that hemorrhage has stopped and that collateral branches penetrating objects, blunt trauma, medical procedures
are not reconstituting the bleeding vessel. In the unlikely (e.g., catheterization), and bone fractures or joint dislo-
event that the common or external iliac artery itself cations.253 Postcatheterization abnormalities include
is lacerated, placement of a stent graft can be curative pseudoaneurysm or AVF formation, dissection, and
(Fig. 8-51). thrombosis. Any long bone fracture can damage a major
A significant fraction of patients with initially nega- artery; posterior knee dislocations are a classic cause of
tive angiography but clinical or imaging evidence for popliteal artery injury254 (Fig. 8-52).
persistent bleeding will show extravasation at repeat Some patients have symptoms that strongly predict
angiography.250 Even bilateral internal iliac artery em- a clinically significant arterial injury (hard signs), in-
bolization is well tolerated in most individuals; the cluding active bleeding, diminished distal pulses, ex-
collateral circulation usually is sufficient to prevent panding or pulsatile hematoma, neurologic deficit, or
ischemia of the pelvic organs. However, buttock and evidence of distal ischemia.255 Others have less convinc-
thigh paresthesia can occur.251 Skin sloughing is rare but ing findings, namely proximity of the injury to a major
can be serious. Sexual dysfunction (which is frequent artery, small hematoma, or unexplained hypotension.
8. PELVIC AND LOWER EXTREMITY ARTERIES 239
C D
AVFs may become apparent long after the traumatic conservatively. Well-accepted indications for imaging
event. include the following255,257,258:
SURGICAL THERAPY
Significant injury to a named artery is sometimes man-
aged by direct repair or bypass graft placement, ideally
with autologous vein. Isolated tibial artery injuries are
sometimes left alone. Many trauma surgeons simply
observe minor vascular injuries such as nonocclusive
intimal flaps, intramural hematomas, small ("1 cm)
pseudoaneurysms, and small asymptomatic AVFs.267
These lesions usually have a benign course.
OTHER DISORDERS
Dissection
Lower extremity arterial dissection most often results from
FIGURE 8-52 Complete popliteal artery occlusion after posterior
extension of an abdominal aortic dissection or a medical
knee dislocation.
procedure such as catheterization (see Chapters 3 and 7).
A B
C D E
FIGURE 8-53 Arteriovenous fistula (AVF) after cardiac catheterization. Color Doppler ultrasound shows a large left groin hematoma
(A) and vessel with turbulent arterial flow (B) suggesting a fistula. C, Selective left iliac arteriography confirms the iatrogenic AVF. In this
unusual instance, the communication is through a small branch (D), which could be catheterized and embolized (E) to abolish the fistula.
limb ischemia and Raynaud phenomenon. The classic an- If the patient continues to smoke, gangrene and
giographic features are abrupt occlusions of tibial and amputation may result. If the patient stops smoking,
pedal arteries with normal intervening segments, tortuous stabilization and some improvement in symptoms can
corkscrew collaterals, and relative sparing of proximal be expected. Pharmacologic treatment with the prosta-
arteries (see Fig. 8-19). cyclin analogue iloprost is effective in some cases.
242 II. AORTA AND PERIPHERAL ARTERIES
A B
C D E
FIGURE 8-54 Traumatic anterior tibial artery pseudoaneurysm from criminal stab wound. A and B, Color Doppler ultrasound shows
a large vascular structure in the right calf with to-and-fro flow characteristic of a pseudoaneurysm. C, Selective angiography confirms the
diagnosis, with origin from the proximal right anterior tibial artery. D, Embolization with coils was done proximally, but later phase of the
arteriogram showed continued pressurization of the pseudoaneurysm through the distal artery via collateral channels (E). At this point,
ultrasound-guided percutaneous thrombin injection was recommended.
Thrombolytic therapy has had mixed results.273 Surgical from any source is partially or completely relieved with
options include sympathectomy, bypass grafting (when vasodilators, removal of the causative factor, and time.
feasible), and, ultimately, amputation. Standing waves are periodic oscillations in an arterial
Vasospasm of the lower extremity arteries is seen with a segment that are occasionally seen during lower ex-
variety of disorders (see Figs. 1-3 and 8-55). Functional tremity CT, MR, or catheter arteriography (see Fig. 1-5).
arterial narrowing occurs when proximal arteries are ob- The regular, corrugated appearance should not be con-
structed. Chronic use or abuse of certain vasospastic fused with other entities. A leading hypothesis invokes
agents can cause ischemic symptoms, diminished pulses, secondary retrograde flow (typical in high resistance
and occasionally gangrene.274 The characteristic finding of arteries) as the explanation for this temporary oscillating
drug-induced vasospasm is bilateral, symmetric, abrupt pattern.275,276
narrowing of the iliac, femoral, or popliteal arteries that Fibromuscular dysplasia is a set of related disorders in
resolves after discontinuation of the drug. Vasospasm which noninflammatory fibrotic tissue proliferates in
8. PELVIC AND LOWER EXTREMITY ARTERIES 243
B C
D E
FIGURE 8-56 Spontaneous retroperitoneal hemorrhage in a patient with sudden onset of back pain and drop in hematocrit. A, Computed
tomography scan shows large heterogenous bleed in left retroperitoneal space. B and C, Abdominal aortography shows a bleeding site (arrow)
but not the source vessel. Sequential arteriography of all left-sided lumbar arteries identified the culprit vessel (D), which was embolized
distally with coils and Gelfoam (E). Bleeding stopped.
8. PELVIC AND LOWER EXTREMITY ARTERIES 245
A B
The precise cause of this disorder is elusive, although may progress to complete occlusion. Standard treatment
it may arise from the adjacent joint capsule, nerve, or is cyst evacuation (with or without patching) or primary
tendon. As the cysts grow and coalesce, they can even- resection. The safety or effectiveness of balloon angio-
tually rupture and narrow (or completely obstruct) the plasty has not been proven.301
arterial lumen. Popliteal artery entrapment syndrome results from
The diagnosis is made with color Doppler sonography chronic, pathologic compression of the popliteal artery
or CT or MR angiography.228,300 The imaging appearance by muscular or tendinous structures within the crowded
is that of smooth, eccentric, extrinsic (hourglass) nar- space of the popliteal fossa.302-304 Transient, functional
rowing of the upper popliteal artery (Fig. 8-59). Stenosis compression of the artery by the soleal sling occurs in
A B C
D E F
FIGURE 8-58 Lateral right knee arteriovenous malformation (AVM) in a young patient. Coronal projection magnetic resonance angiogra-
phy in early (A) and later phase (B) shows the complex highly vascular lesion on the lateral side of the right knee. Multiple parallel channels
reflect rapid arterial inflow and venous outflow from the AVM. C and D, Selective catheter arteriography confirms the findings of an enlarged
right popliteal artery and rapid arteriovenous shunting. E and F, Superselective catheterization of a dominant feeding branch followed by
injection of Onyx to penetrate into the nidus (arrows).
8. PELVIC AND LOWER EXTREMITY ARTERIES 247
G H I
J K L
FIGURE 8-58, contd G, Postembolotherapy arteriography shows markedly decreased vascularity to the AVM. Patients symptoms were im-
proved but persisted. Follow-up arteriography (H and I) with superselective catheterization (J) of a more superior dominant feeding artery
shows residual malformation. K and L, Postembolotherapy angiography shows further reduction in extent of disease.
248 II. AORTA AND PERIPHERAL ARTERIES
A B
FIGURE 8-59 Cystic adventitial disease of the popliteal artery. A, T2-weighted transverse magnetic resonance image shows a cystic lesion
(arrow) compressing the normal popliteal artery. B, Catheter angiogram reveals the classic hourglass appearance of the lesion. (Courtesy of
Thomas Velling, MD, Newport Beach, Calif.)
8. PELVIC AND LOWER EXTREMITY ARTERIES 249
A B
C D
FIGURE 8-60 Popliteal artery entrapment syndrome. A, Color Doppler ultrasound of right popliteal fossa shows widely patent artery. B, With
active plantar flexion of the ankle, the artery is occluded. Selective left leg arteriography shows a normal popliteal artery at rest (C), but complete
compression with active plantar flexion (D).
250 II. AORTA AND PERIPHERAL ARTERIES
B
FIGURE 8-61 Iliac artery endofibrosis with claudication in a high-performance cyclist. A, Oblique pelvic arteriography shows short
segment proximal narrowing of the left external iliac artery (arrow). Note standing waves below this level; this is a functional phenomenon.
B, Ultrasound at the level of the affected artery shows typical heaped-up arterial wall causing only minimal narrowing at rest.
Neoplasms
only seen in high-performance athletes (particularly
racing cyclists)308-311 (Fig. 8-61). The cause is unknown. Catheter angiography has almost no role in the evaluation
Patients are only symptomatic with vigorous activity. of neoplasms of the lower extremity. Occasionally, patients
Screening is done with segmental blood pressure mea- with highly vascular tumors undergo arteriography as
surements during and after extreme exercise. Sonogra- part of an embolization procedure to minimize bleeding
phy or CT angiography confirms the diagnosis. The during surgery. Women with gynecologic tumors compli-
standard treatment is saphenous vein patch angioplasty cated by pelvic or vaginal bleeding may also be treated
or bypass graft placement.310 with embolotherapy (see Chapter 13).
8. PELVIC AND LOWER EXTREMITY ARTERIES 251
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pression in a normal population. J Vasc Surg 1994;20:978. fibrosis: a new possible predisposing factor. J Vasc Surg 2003;
306. Hai Z, Guangrui S, Yuan Z, et al. CT angiography and MRI in 38:180.
patients with popliteal artery entrapment syndrome. AJR Am J 310. Abraham P, Bouye P, Quere I, et al. Past, present and future of
Roentgenol 2008;191:1760. arterial endofibrosis in athletes: a point of view. Sports Med
307. Zhong H, Liu C, Shao G. Computed tomographic angiography 2004;34:419.
and digital subtraction angiography findings in popliteal artery 311. Giannoukas AD, Berczi V, Anoop U, et al. Endofibrosis of iliac
entrapment syndrome. J Comput Assist Tomogr 2010;34:254. arteries in high-performance athletes: diagnostic approach and
308. Vink A, Bender MH, Schep G, et al. Histopathological compari- minimally invasive endovascular treatment. Cardiovasc Intervent
son between endofibrosis of the high-performance cyclist Radiol 2006;29:866.
and atherosclerosis in the external iliac artery. J Vasc Surg
2008;48:1458.
C H A P T E R
9
Upper Extremity Arteries
Karim Valji
ANATOMY
(ONLINE CASES 3 AND 17)
Development
In early gestation, the upper limbs are nourished by
the axial artery. This vessel evolves into the axillary,
brachial, interosseous, and median arteries that feed
the hand in the fetus.1 The ulnar artery is an out-
growth of the brachial artery at the elbow. The radial
artery arises from a superficial branch of the proximal
brachial artery, but its origin migrates toward the
elbow as the fetus grows. In most cases, the distal
interosseous and median arteries regress before birth.
Normal Anatomy
FIGURE 9-1 Steps in catheterization of the arch vessels with The subclavian arteries originate from the brachiocephalic
a headhunter catheter. The catheter can then be advanced into the (innominate) artery on the right and directly from the aortic
right subclavian artery over a guidewire. Further withdrawal of
the catheter (third panel) will cause it to jump into the left common
arch on the left2 (Fig. 9-3). The artery runs posterior to the
carotid and then into the left subclavian artery. (Adapted from Kadir S. subclavian vein and the anterior scalene muscle. It arches
Diagnostic angiography. Philadelphia: WB Saunders, 1986:177.) over the pulmonary apex within the costoclavicular space
259
260 II. AORTA AND PERIPHERAL ARTERIES
Humeral
circumflex
arteries
Brachial artery
Deep brachial
artery
Ulnar collateral
FIGURE 9-5 Right internal thoracic (mammary) arteriography. arteries
The vessel continues as the superficial epigastric artery as it enters
the abdomen (arrow).
Interosseous
recurrent
artery
arteries. These branches supply muscles of the shoulder
girdle, humerus, scapula, and chest wall. Radial recurrent Ulnar recurrent
artery arteries
At the lateral edge of the teres major muscle (approxi-
mately the lateral scapular border), the axillary artery
becomes the brachial artery. In the mid-upper arm, the
artery lies in a fascial sheath along with the basilic vein,
Ulnar artery
paired brachial veins, and the median and ulnar nerves.
Its major branches include the deep brachial and the supe-
Radial artery
rior and inferior ulnar collateral arteries (Fig. 9-6). At Interosseous
about the level of the radial head, the brachial artery di- arteries
vides into the radial and ulnar arteries (Fig. 9-7). The radial
artery obviously descends on the radial side of the fore-
arm. The ulnar artery, which is usually the larger of the FIGURE 9-6 Arterial anatomy and collateral circulation of the
two, gives off the common interosseous artery and then upper arm and elbow.
descends on the ulnar side of the forearm. The interosseous
artery divides into anterior and posterior branches sepa-
rated by the interosseous membrane. In less than 10% the wrist. The superficial arch is dominant and typically
of individuals, the anterior interosseous or median artery forms distal to the deep arch. The princeps pollicis and
persists and contributes to the palmar arch.3 radialis indicis arteries arise from the radial artery and
The arterial anatomy of the hand is extremely variable, supply the thumb and index finger, respectively. The
and deviations from the classic pattern described here are superficial palmar arch gives off three or four common
common.3,4 The ulnar artery supplies the superficial palmar palmar digital arteries, and the deep arch gives off the
arch, and the radial artery supplies the deep palmar arch palmar metacarpal arteries. At the bases of the proximal
(Figs. 9-8 and 9-9). The arches often are in continuity with phalanges, adjacent metacarpal vessels from each arch
the opposing forearm artery through small branches at merge and then immediately divide into proper digital
262 II. AORTA AND PERIPHERAL ARTERIES
Palmar arteries
Proper Superficial
digital arch
arteries
Deep
arch
R
Metacarpal
arteries
Princeps
I pollicis
artery
U
MAJOR DISORDERS
extremity arterial obstruction causes abrupt onset of arm circulation is robust. The presence of arm swelling
pain, coolness, cyanosis, pallor, diminished or absent should raise the suspicion of severe venous thrombosis
pulses, and, occasionally, sensorimotor deficits. How- (see Chapter 17).
ever, some patients are only mildly symptomatic if the
underlying disease is chronic (as with thrombosis at a Imaging
site of preexisting atherosclerotic stenosis) and collateral Duplex sonography, computed tomography (CT) angi-
ography, and magnetic resonance (MR) angiography
are sometimes used in the initial evaluation of patients
who do not go directly for operation11-13 (Fig. 9-12).
BOX 9-1 Catheter angiography is usually reserved for cases in
which endovascular treatment is planned. It is cus-
SOURCES OF UPPER tomary to investigate the entire circulation from the
E X T R E M I T Y A RT E R I A L aortic arch to the digital arteries of the hand to identify
EMBOLI potential sources of emboli and to search for occult
distal disease. An acute embolus produces a discrete
Cardiac thrombus (e.g., left atrium in atrial
filling defect with reconstitution of the distal vessels.
fibrillation)
However, it also may appear as a sharp cutoff that mim-
Atherosclerotic plaque in aortic arch or proximal
ics a thrombotic occlusion (Fig. 9-13). After the embolic
arteries
event occurs, clot propagates proximally and distally to
Aneurysm thrombus (e.g., subclavian artery)
the next large collateral branches. Post-traumatic throm-
Proximal in situ thrombosis from thrombophilic
bosis results in an abrupt occlusion at or near the site
state
of injury (Fig. 9-14).
Trauma
Endocarditis Treatment
Paradoxical embolus from venous circulation
Blood flow to the arm must be restored promptly (within
through right to left shunt
about 4 to 6 hours after acute occlusion in the absence
of preexisting collateral circulation) to avoid ischemic
B C
FIGURE 9-12 Brachial artery embolus. A, On contrast computed tomography angiography, the patent right brachial artery (arrow) becomes
filled with thrombus on more distal image (B, arrow). C, On a reformatted image, the short segment brachial artery occlusion (arrows) is
depicted.
9. UPPER EXTREMITY ARTERIES 265
A D
C F
G H
I
FIGURE 9-13 Embolus to the left brachial artery in a patient with thoracic outlet syndrome. A through C, Contrast-enhanced computed
tomography images show left subclavian artery (arrow) abutting callus from an old clavicular fracture with post-stenotic dilation of the artery
(arrow). Unlike the right brachial artery (arrowhead), the mid left brachial artery is thrombosed (curved arrow). D, Left subclavian arteriogram
shows mural thrombus within the dilated segment of the left subclavian artery (large arrow) and complete occlusion of the proximal left
brachial artery (small arrow). E, Weak collateral flow is found in the upper arm. F, Following overnight thrombolysis with t-PA at 1 mg/hr, the
proximal occlusion is completely gone. Flow is noted to the distal left brachial artery (G), with collateral filling of forearm arteries (H). I, With
the left arm in extreme abduction, narrowing of the subclavian artery is noted (arrow).
266 II. AORTA AND PERIPHERAL ARTERIES
A B
Clinical Features
Most patients with atherosclerosis-related thrombosis
are older than 50 years of age. Chronic obstructions of the
subclavian and axillary arteries may be entirely asymp-
tomatic. Similar percentages of patients suffer arm
ischemia and neurologic problems. Arterial obstructions
are associated with ischemic symptoms such as exer-
tional arm pain (claudication), and less commonly rest
pain or tissue loss. Pulse deficits and blood pressure
differences between the two arms (usually "20 mm Hg
systolic) should be sought. Many individuals have neu-
rologic symptoms related to subclavian steal, including
dizziness, syncope, visual disturbances, or ataxia. Those
with coronary-subclavian steal are at risk for developing
angina during arm exercise. Finally, thoracic outlet syn-
drome is a common cause of arm ischemia, particularly
in younger individuals (see later discussion).
FIGURE 9-16 Coronary-subclavian steal in a patient with a left Imaging
internal mammary artery (LIMA) coronary bypass graft. Early phase
of arch aortogram shows occlusion at the origin of the left subclavian Duplex sonography, CT angiography, and MR imaging
artery (arrow) and retrograde flow up the LIMA (curved arrow) into (MRI) play a role in evaluation of patients with sus-
the mid left subclavian artery. pected proximal arterial obstruction, particularly when
268 II. AORTA AND PERIPHERAL ARTERIES
they have symptoms of subclavian steal.11-13,28 Doppler transposition, axilloaxillary bypass, or subclavian-
ultrasound signs of obstructive disease include a parvus subclavian bypass.29,38 Brachial artery revasculariza-
et tardus waveform (downstream lesion) and loss of tion is done with autologous vein or synthetic graft
normal diastolic flow reversal (upstream lesion).11 material.39
Catheter angiography is performed when noninva-
sive imaging studies are equivocal (a rare situation) Thoracic Outlet Syndrome
or endovascular therapy is contemplated. Atheroscle-
rotic stenoses are typically found at the origins of the Etiology
subclavian or brachiocephalic arteries (see Fig. 9-15). The various forms of thoracic outlet syndrome are a
With proximal subclavian artery obstruction, flow in the distinct set of clinical disorders of the upper extremity
ipsilateral vertebral artery may be reversed. Thrombotic caused by extrinsic compression of the major nerves and
occlusions produce an abrupt vessel cutoff. Arterio- blood vessels exiting or entering the thorax. In more
graphic findings in thoracic outlet syndrome and more than 90% of affected persons, symptoms are caused by
unusual causes of chronic obstruction are considered in compression of the brachial plexus and related nerves;
later sections. arterial compression is responsible for less than 5%
of cases.40-42 However, these frequently reported figures
are strongly influenced by the composition of referral
Treatment
patterns.
ENDOVASCULAR THERAPY The subclavian and axillary arteries are subject
When feasible, catheter-based interventions (usually to compression primarily within three well-defined
primary stent placement) are preferred for subclavian anatomic regions: the interscalene triangle, costocla-
and brachiocephalic artery obstructions.24,29-32 In a mi- vicular space, and retropectal (subcoracoid) space
nority of cases, direct brachial artery puncture is neces- (Fig. 9-17). Imaging studies in normal volunteers
sary instead of (or combined with) femoral artery access: show that a significant minority of healthy individuals
For proximal left subclavian and brachiocephalic
artery stenosis, current practice favors primary
stent placement to improve long-term durability.
However, data supporting this approach (rather
than stent placement for immediate angioplasty
failure) are weak. Both technical success (#90%)
and long-term results (almost 90% primary
patency at 10 years in one large series) are
excellent.32-36 Adverse events are uncommon,
and neurologic events are rare.
Balloon angioplasty alone may be performed
in the central segment of the subclavian arteries.
If a stent is absolutely necessary, only the self-
expanding variety should be considered because
of the potential for extrinsic compression by
adjacent musculoskeletal structures.
Treatment is indicated for patients with significant
arch vessel obstructions before planned internal
thoracic artery bypass to the coronary arteries.
Thrombolysis has virtually no role in chronic
total brachiocephalic and subclavian artery occlu-
sions. Balloon angioplasty alone is not durable.37
If such lesions can be crossed with a guidewire,
primary stent placement (if at a suitable site) is
warranted.
SURGICAL THERAPY
The preferred operative method for treating total sub- FIGURE 9-17 The major sites of arterial compression in thoracic
clavian artery occlusion is an extrathoracic bypass proce- outlet syndrome are (medial to lateral) the scalene triangle,
dure, such as carotid-subclavian bypass, carotid-subclavian costoclavicular space, and subcoracoid (retropectal) space.
9. UPPER EXTREMITY ARTERIES 269
exhibit arterial constriction within the costoclavicular venous) compression along the thoracic outlet. More
and retropectal spaces with arm elevation.43,44 In a flagrant findings may also be seen, including post-
small number of patients, however, this physiologic stenotic arterial dilation, aneurysm formation with or
narrowing is exaggerated by one of several musculo- without mural thrombus, distal embolization, or com-
skeletal abnormalities. These include cervical ribs, plete thrombosis. MR angiography is particularly help-
elongated C7 transverse processes, and congenital or ful in assessing the brachial plexus and fibromuscu-
acquired pathology of the first rib or clavicle.45 Some- lar abnormalities affecting the blood vessels. Duplex
times, soft tissue abnormalities alone (e.g., congeni- sonography is a complementary tool, but it has distinct
tal fibromuscular bands, muscular hypertrophy) are limitations compared with MR and CT.44,45 It is impor-
responsible. tant to realize that compression of the subclavian artery
Chronic and intermittent arterial compression, which during provocative maneuvers has been identified in a
is usually exacerbated by particular arm positions, can substantial percentage of normal volunteers by Doppler
lead to intimal and ultimately transmural vascular in- sonography.44
jury. Over time, the result is post-stenotic dilation or
frank aneurysm formation, premature atherosclerosis, CATHETER ANGIOGRAPHY
embolization of platelet-fibrin deposits or thrombus This procedure is only required for assessment of forearm
from the diseased wall, or complete occlusion. or hand arteries (if CT or MR angiography is not diag-
nostic) and when endovascular therapy is contemplated.
Clinical Features Arteriographic findings mirror those described above
Thoracic outlet syndrome is classically seen in young with cross-sectional imaging (see Fig. 9-13). With com-
or middle-aged adults.46 The arterial form of the disease plete thrombosis of the subclavian or axillary artery, an
causes arm pain, weakness, coolness, and pallor. Symp- underlying abnormality rooted in thoracic outlet syn-
toms often are intermittent and usually provoked by drome may only be revealed after thrombolytic therapy
certain arm positions or exercise. There may be evidence (Fig. 9-18).
for distal embolization, such as digital ulcerations or
cyanosis. With associated arm swelling, the venous form
Treatment
of thoracic outlet syndrome should be considered (see
Chapter 17). ENDOVASCULAR THERAPY
A host of shoulder movements are reported to repro- Thrombolysis may be used to recanalize an acutely
duce symptoms in some individuals, including the occluded artery from suspected thoracic outlet syndrome
Adson maneuver (i.e., depression of the shoulder with (see Figs. 9-13 and 9-18). After flow is restored, antico-
the head turned to the symptomatic side), military posi- agulation is begun. Later, the underlying compressive
tion (i.e., shoulders hyperflexed), hyperabduction of the abnormality is treated operatively. Stents should not be
arm, and the so-called surrender position (hands above placed at the site of compression.49
the head).45 However, loss of the radial pulse with
extreme abduction of the arm is normal in a minority of SURGICAL THERAPY
the population and is not itself diagnostic of the disease. For patients with mild symptoms and an imaging
Frankly, it may be difficult to distinguish neurogenic study showing normal subclavian and axillary arteries
from arterial thoracic outlet syndrome, and sometimes or only mild post-stenotic dilation in the neutral posi-
they coexist. tion, conservative therapy is often appropriate. For
individuals with disabling symptoms, florid imaging
findings, or distal embolization, surgery usually is per-
Imaging
formed.49 The underlying musculoskeletal abnormality
PLAIN RADIOGRAPHY is corrected (e.g., removal of a cervical rib, release of
Chest or cervical spine radiographs are inspected for fibrous bands) along with resection of the first rib.41,42
cervical ribs or other bony abnormalities often found Subclavian artery aneurysms are treated by resection
with arterial thoracic outlet syndrome. and bypass.
CROSS-SECTIONAL TECHNIQUES
Digital Ischemia (Online Case 56)
MR angiography and CT angiography are the primary
modalities used to evaluate these patients43,45-48 (see Etiology
Fig. 9-13). When thoracic outlet syndrome is suspected, Ischemia of the digits may be caused by fixed obstruc-
imaging is done first with the arms at the side and then tions of large or small arteries, intermittent vasospasm, or
with the arm extended above the head. Sagittal refor- both. Obstruction of large or medium-sized arteries alone
mations are especially useful in depicting arterial (or occasionally produces digital ischemia (see Box 9-2). More
270 II. AORTA AND PERIPHERAL ARTERIES
often, the ischemia is caused by small vessel disease in the The mechanisms underlying distal hypoperfusion isch-
hand50 (Box 9-3). Raynaud phenomenon refers to functional emic syndrome (dialysis access-related digital artery in-
vasoconstriction of the small arteries of the hand (and less sufficiency) are several27:
often the feet) with certain stimuli (e.g., cold, emotional
Obstructive disease within the access inflow or
stress).51 Raynaud disease refers to this form of intermit-
outflow artery
tent, reversible ischemia in the absence of fixed arterial
Steal phenomenon, including retrograde flow
obstructions.52-54
through the ulnar artery via palmar arches
Emboli to the palmar and digital arteries may arise
Inadequate reactive collateral flow development,
from many sources, including the heart, atherosclerotic
sometimes related to arterial mural calcification
plaque (usually in the subclavian artery), subclavian
artery aneurysms (often related to thoracic outlet syn- Chronic, repetitive trauma to the hand, often from vibra-
drome), arterial injury, endocarditis, and thrombosed tory activity or repetitive pounding, can lead to intimal
hemodialysis grafts.26 Buerger disease is considered in a injury and eventual occlusion of palmar arteries. In these
later section in this chapter. patients with hypothenar hammer syndrome, trauma to the
distal ulnar artery as it runs across the hook of the hamate
can progress to aneurysm formation, occlusion, and distal
embolization.55,56 A similar disorder of the distal radial artery
has also been described (thenar hammer syndrome).57
BOX 9-3 Digital ischemia is relatively common in patients with
certain collagen-vascular diseases. These heterogeneous
C AU S E S O F O B S T R U C T I V E disorders produce intimal thickening of small arteries of
A RT E R I A L D I S E A S E O F the wrist and hand that can lead to complete occlusion.58,59
THE HAND By itself, atherosclerosis of the small arteries of the arm
and hand rarely causes symptomatic digital ischemia.
Emboli
However, patients with chronic renal failure are prone to
Buerger disease
accelerated atherosclerotic disease of the digital arteries.60
Diabetes
The radial artery is sometimes harvested as a conduit
Trauma
for coronary artery bypass grafting.61 Acute ischemia is
Vibrational or pounding injuries
rare, and numbness and paresthesias occur in less than
Thermal injury (e.g., electrical burns, frostbite)
10% of cases.
Collagen-vascular diseases
Scleroderma Clinical Features
Rheumatoid arthritis
Patients with occlusions of the palmar or digital artery
Systemic lupus erythematosus
present with moderate to severe pain in the hand and
Atherosclerosis
fingers (which may be exacerbated by cold or stress),
Chronic renal failure
finger ulcerations, or even gangrene. Bluish discolor-
Thrombophilic states
ation of one or more fingers (blue digit syndrome) sug-
Idiopathic sources
gests microembolization of platelet-fibrin or cholesterol
deposits from a proximal source. Many patients have a
9. UPPER EXTREMITY ARTERIES 271
history of tobacco use, collagen-vascular disease, diabe- embolization from the heart or ascending aorta, pro-
tes, chronic hand trauma (e.g., in karate enthusiasts duce angiographic abnormalities in both hands even if
or jackhammer users), or cardiac disease. Noninvasive symptoms are confined to one side.
studies, including finger and arm pressure measure- The angiographic findings depend on the underlying
ments, Doppler flow studies, and plethysmography, are disorder.65 When embolization is suspected, a careful
important in the diagnostic workup of these patients. search for a proximal source should be made (Fig. 9-20).
Still, the diagnosis of embolism can be made with confi-
Imaging dence only if discrete intraluminal filling defects are
The purpose of imaging is three fold: found. The collagen-vascular diseases typically strike
the mid to distal forearm and proper digital arteries
To identify emboli, which will require anticoagu-
(Fig. 9-21). Focal occlusion or an aneurysm of the ulnar
lant therapy and/or exclusion of the offending
artery near the hook of the hamate is diagnostic of
proximal source
hypothenar hammer syndrome (Figs. 9-22 and 9-23).
For specific diagnosis when prognosis is
The arteriographic findings in Buerger disease are
important (e.g., Buerger disease)
considered later. Atherosclerosis produces stenoses
To localize treatable disease that may improve
and occlusions of the digital arteries with less severe
circulation to the hand
disease in the palmar vessels. For patients with sus-
With current state-of-the-art contrast-enhanced angiog- pected Raynaud phenomenon, angiography should be
raphy and 3T capability, MRI nearly approaches the di- performed before and after injection of a vasodilator.
agnostic quality of catheter arteriography62-64 (Fig. 9-19).
When catheter angiography is deemed necessary, a
Treatment
comprehensive study from the aortic arch to the digital
arteries of the affected hand should be performed. Intra- MEDICAL/SURGICAL THERAPY
arterial vasodilators often are given beforehand to relieve Many patients who present with chronic digital ischemia
functional vasospasm. Some interventionalist perform have little or no further progression of their symp-
bilateral hand arteriography even if the symptoms are toms.50,58 For these patients, medical treatment with anti-
unilateral. Most of the systemic disorders, including coagulants, antispasmodic agents, or both is appropriate.
A B
272 II. AORTA AND PERIPHERAL ARTERIES
A B
ENDOVASCULAR THERAPY
Thrombolytic therapy has been used occasionally in
FIGURE 9-21 Scleroderma is characterized by abrupt occlusions
of multiple proper digital arteries. The distal radial and ulnar arteries some cases of acute or subacute arterial occlusion in the
are occluded. Note prior second digit amputation. hand.16,69,70
A B
Imaging
Over the past several decades, there has been a gradual
evolution in the approach to suspected upper extremity
arterial damage. Protocols for routine surgical explora- BOX 9-5
tion or arteriography for all proximity injuries have
I N D I C AT I O N S F O R
been abandoned.80 After clinical evaluation, some pa-
VA S C U L A R I M A G I N G
tients with hard signs of injury go directly to operation
AFTER UPPER EXTREMITY
without imaging studies. In most cases, an ankle-
T R AU M A
brachial index (ABI) or Doppler arterial pressure index
(API, ratio of distal pressure in affected versus unaf-
Hard signs of vascular injury
fected arm) is determined. In the absence of hard signs
Obvious arterial bleeding
of injury or in the presence of API or ABI greater than
Expanding hematoma
0.90, patients are usually observed.77
Absent or markedly diminished distal pulses
SONOGRAPHY Ischemic symptoms
Bruit or thrill
In some centers, patients with suspected extremity arterial
Neurologic deficit
injuries are routinely evaluated with color Doppler sonog-
Shock in absence of other injuries
raphy.78,79 In patients at low risk for significant pathology,
Shotgun blast
the accuracy exceeds 95% in recent reports. Pitfalls of the
History of peripheral vascular disease
technique include limited evaluation of the thoracic outlet
Thoracic outlet injury
and confusion in the face of variant anatomy. Sonography
Extensive bone or soft tissue injury
is useful also for delayed diagnosis of post-traumatic
Delayed presentation
pseudoaneurysms and arteriovenous fistulas, particularly
in the subclavian and axillary arteries (Fig. 9-24).
274 II. AORTA AND PERIPHERAL ARTERIES
A B
B C
FIGURE 9-25 Subclavian artery pseudoaneurysm resulting from attempted venous access placement without imaging guidance.
A through C, Axial and reformatted coronal contrast-enhanced computed tomography of the upper chest shows a pseudoaneurysm
(large arrow) arising from the mid right subclavian artery (small arrow). There is some surrounding soft tissue density suggesting the
presence of blood.
SURGICAL THERAPY
Significant injuries to major arteries, such as occlusion,
laceration, pseudoaneurysm, and flow-limiting dissec-
tion, require surgical treatment with resection or bypass
grafting if not amenable to endovascular techniques.96-98
Time is of the essence in repairing occlusive injuries.
Permanent ischemic injury can result if revasculariza-
tion is not accomplished within about 4 to 6 hours
of proximal injury (somewhat longer for more distal
occlusions).14 The current trend is toward conservative
management of minor vascular injuries such as nonoc-
clusive intimal flaps, intramural hematomas, and small
(%1 cm) pseudoaneurysms.87 These lesions generally
have a benign clinical course.
B C
D E
FIGURE 9-27 Older man with hypotension after a fall. A, Computed tomography scan shows swelling and high density in left
shoulder girdle muscles, suggesting active bleeding. B, Left subclavian arteriography shows a pseudoaneurysm arising from a branch of the
costocervical trunk, confirmed with selective catheterization (C). D, Coaxial microcatheter advanced to the inflow branch. E, Following
embolotherapy across the aneurysm neck with microcoils and Gelfoam pledgets, bleeding has stopped.
puncture, radial artery line placement, or attempted symptoms from distal embolization or aneurysmal
vascular access placement in the subclavian or jugular thrombosis or have hypotension from rupture. Rarely,
vein (see Fig. 9-28). Aneurysms can develop near the site patients suffer massive hemoptysis after erosion into
of extrinsic compression in patients with TOS (see Fig. the lung.
9-18). In the hand, aneurysms usually are caused by
penetrating trauma or chronic blunt trauma (e.g., hypo- Imaging and Treatment
thenar hammer syndrome). Microaneurysms of small Duplex sonography, CT angiography, and MR angiog-
vessels of the hand are characteristic of a necrotizing raphy are used to diagnose central aneurysms100,101
vasculitis such as polyarteritis nodosa. (see Figs. 9-24 and 9-28). Color Doppler sonography
Subclavian artery aneurysms often are asymptomatic. is valuable for detecting aneurysms of the brachial,
Some patients present with chest pain, shoulder pain, or forearm, and hand arteries.102 Catheter angiography
a pulsatile supraclavicular mass. Others complain of usually is reserved for cases in which percutaneous
9. UPPER EXTREMITY ARTERIES 277
A C
D E F
FIGURE 9-28 Balloon tamponade of inadvertent subclavian artery puncture for central venous catheter placement. A, Chest radiograph
shows the access line in place (small arrow). Pulsatile blood was obtained from the catheter. B and C, Axial computed tomography images
confirm that the catheter is in the right subclavian artery (small arrows). D, Transfemoral subclavian arteriography identified the entry site of
the errant catheter (large arrow). E, Via transbrachial access, a balloon is inflated across the vessel puncture site after the catheter was removed
but guidewire left in place. F, Final subclavian arteriogram shows that the artery is normal and no leak is evident.
therapy is being considered. Degenerative aneurysms, post-traumatic aneurysms is described previously. Stent
which are typically located in the brachiocephalic grafts may play a role in rare instances.
or subclavian arteries, usually are fusiform and calcified.
Traumatic or infectious pseudoaneurysms are typically
saccular, irregular, or multilobed (see Figs. 9-22, 9-24, OTHER DISORDERS
9-25, and 9-27). Aneurysms caused by connective tissue
disorders or vasculopathies may be fusiform or saccular
Vasculitis and Vasculopathies
(Fig. 9-29).
The standard treatment for upper extremity arterial Several vasculitides and noninflammatory vasculopathic
aneurysms is surgical resection with end-to-end anasto- states affect the upper extremity arteries (Fig. 9-30). Their
mosis or bypass grafting.103 Percutaneous therapy for pathogenesis is considered in more depth in Chapter 1.
278 II. AORTA AND PERIPHERAL ARTERIES
Arteriovenous Communications
Vascular anomalies and techniques for percutaneous
treatment are discussed in greater detail in Chapters 1
and 3. This set of disorders encompasses vascular mal-
formations, including arteriovenous malformations
(AVMs), venous malformations (VM), and lymphatic
malformations (LM), hemangiomas, and arteriovenous
fistulas (AVFs). AVFs are almost always acquired from
accidental or iatrogenic trauma. Congenital AVMs and
VMs and hemangiomas are conditions that also may
FIGURE 9-29 Brachial artery aneurysm in a patient with affect the upper extremity.114-117 Most patients with
Ehlers-Danlos syndrome. these lesions present as children or young adults with
9. UPPER EXTREMITY ARTERIES 279
B C
D E
FIGURE 9-30 Subclavian artery aneurysm in a patient with neurofibromatosis. A, Chest radiograph shows innumerable cutaneous
neurofibromas. B and C, Right brachiocephalic arteriography shows a bilobed aneurysm (single arrow) with massive extravasation into the
chest (double arrows). The relationship to the vertebral artery must be determined. D, A covered stent was inserted in proper position, but leak
persists (arrow). E, The stent graft was slightly overdilated, now sealing the pseudoaneurysm and eliminating the leak. Vertebral artery patency
was maintained (arrow).
280 II. AORTA AND PERIPHERAL ARTERIES
Neoplasms
Arteriography has virtually no role in the evaluation
of patients with benign or malignant tumors of the
shoulder or arm. Occasionally, patients with highly
vascular tumors undergo arteriography for preoperative
planning or for embolotherapy to reduce blood loss
during surgery.
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S E C T I O N III
10
Renal Arteries and Veins
Karim Valji
ARTERIOGRAPHY splanchnic branches of the aorta begin to perfuse struc-
AND VENOGRAPHY tures arising from the mesonephric ridge: adrenal
(ONLINE VIDEOS 10-1 AND 10-2) glands, gonads, and kidneys. With the ascent of the kid-
neys to the midabdomen, they are ultimately supplied
Evaluation of the renal arteries begins with abdominal by the more caudal of these lateral splanchnic arteries.
aortography to detect renal artery ostial disease and ac- Anomalies in the location and number of renal arteries
cessory arteries before selective catheterization is done. can be explained by incomplete regression of some of
A 4- or 5-French (Fr) pigtail catheter (or similar configu- these primitive vessels.
ration) is positioned with the side holes at the level of
the main renal arteries (approximately the L1 or L2 ver-
tebral body). Images are routinely obtained in an antero-
Normal Anatomy
posterior or slight right posterior oblique views.1 If The renal arteries arise from the lateral surface of the
computed tomography (CT) or magnetic resonance aorta at about the L1-L2 vertebral level.8,9 The right renal
(MR) angiograms are available, they will guide selection artery runs posterior to the inferior vena cava (IVC) and
of an optimal projection to place the renal artery origins right renal vein to enter the renal hilum. The left renal
in profile or may replace the catheter aortogram. artery passes behind the left renal vein. The proximal
Selective renal arteriography is performed with a 4- or renal arteries have small inferior adrenal, ureteric, and
5-Fr cobra or reverse curve (e.g., Sos or Simmons) catheter. capsular branches, which often are not seen on imaging
The average flow rate in a normal renal artery is 5 to 6 mL/ studies. At the renal hilum, the artery bifurcates into
sec. More distal catheterization is done with coaxial micro- dorsal and ventral rami (Fig. 10-1). These trunks sepa-
catheters and microwires. Because the renal artery and its rate into segmental branches, which then further divide
branches are prone to vasospasm and dissection, guidewires into lobar branches supplying the renal pyramids. The
and catheters should be manipulated with extreme care. vessels successively branch into the interlobar, arcuate,
Renal venography is accomplished with a straight and interlobular arteries. In the renal cortex, the inter-
catheter (e.g., cobra shape) or reverse curve catheter (e.g., lobular arteries divide into afferent arterioles that
Simmons 2). Valves at the origin of the veins may cause supply the glomeruli.
resistance to catheter passage. The valves can always be The renal venous system follows a branching
crossed with gentle guidewire probing. A wire may be pattern similar to that of the renal arteries. However,
required to seat the catheter well within the vein. wide anastomoses exist among the intrarenal veins
In patients with renal dysfunction (serum creatinine (Fig. 10-2). Both main renal veins run in front of their
level greater than 1.2 to 1.5 mg/dL), various measures corresponding arteries. The right renal vein passes be-
are taken to minimize the risk of contrast-induced hind the duodenum and enters the right lateral surface
nephropathy2-6 (see Chapter 2). of the IVC.10 The left renal vein, which is about three
times as long, runs between the aorta and superior
mesenteric artery and then drains into the left lateral
ANATOMY wall of the IVC. The left gonadal vein enters the left renal
vein along its undersurface just to the left of the spine
(Fig. 10-3). The left adrenal vein enters the left renal vein
Development
on its superior surface usually in a combined trunk
In the fetus, the kidneys lie in the pelvis and receive with the left inferior phrenic vein. The right adrenal and
blood from neighboring vessels, including the median gonadal veins typically have separate entrances into
sacral and common iliac arteries.7 With time, lateral the IVC at or near the origin of the right renal vein
287
288 III. VISCERAL ARTERIES AND VEINS
FIGURE 10-1 Arteriogram of a normal right kidney. FIGURE 10-3 Normal left renal venogram with partial filling of
the left phrenicoadrenal trunk (thick arrow) and gonadal vein to the
level of the first valve (thin arrow).
A B
A B C
FIGURE 10-4 A, Accessory right and left renal arteries (arrows). B, In another patient, a small artery above the left renal artery is noted.
C, Selective injection indicates an accessory renal artery feeding the lower pole.
Collateral Circulation
With renal artery stenosis or occlusion, an extensive col-
lateral circulation maintains blood flow to the kidney.
Although renal arteries have been described as end
arteries, communications between extrarenal arteries
and segmental, interlobar, and arcuate vessels do exist.
The classic description of collateral arterial flow in the
kidney was made by Abrams and Cornell.20 The intrare- B
nal vessels are primarily supplied by three collateral
networks: the capsular, peripelvic, and periureteric FIGURE 10-5 Accessory right renal artery. A, Contrast-enhanced
computed tomography shows main right renal artery (arrow). B, An
arteries. These three systems are ultimately fed by
accessory right renal artery exits the aorta above the main vessel
the lumbar arteries, aorta, internal iliac artery, inferior (arrow).
adrenal artery, and other vessels (Fig. 10-10).
In main renal vein obstruction, venous outflow
occurs through ureteral, gonadal, adrenal, ascending
lumbar, and capsular venous pathways (Fig. 10-11).
290 III. VISCERAL ARTERIES AND VEINS
A B
FIGURE 10-6 Accessory right renal artery. A, Injection of the main artery demonstrates the beaded appearance of fibromuscular dysplasia
(arrowhead). In addition, it shows no crossing of vessels in the hilum and indistinct nephrogram in mid and lower pole, suggesting the presence of
an additional artery feeding the dorsal aspect of the kidney (B). Also note prominent capsular arteries (arrow).
MAJOR DISORDERS
B C
FIGURE 10-8 Circumaortic left renal vein. A, Gadolinium-enhanced magnetic resonance angiogram shows main left renal vein (arrow)
entering the inferior vena cava (IVC). B, Circumaortic component passes behind the aorta to join the IVC (arrow). C, Maximum intensity
projection demonstrates the orthotopic and circumaortic (C) left renal veins.
B
292 III. VISCERAL ARTERIES AND VEINS
A B
FIGURE 10-11 Venous collaterals with chronic left renal vein FIGURE 10-12 Nephrosclerosis of the left kidney. Note irregu-
stenosis caused by impingement between the superior mesenteric larity and pruning of distal intrarenal branches (compare with
artery and aorta (nutcracker phenomenon). Fig. 10-1).
contributes to elevated blood pressure. RVH is reported minor factor in development of chronic kidney disease
in about 3% to 5% of cases of hypertension in the general compared with microvascular changes caused by diabe-
population, although this figure is hotly debated.22 tes, hyperlipidemia, or hypertension itself.24 Finally, the
Ischemic nephropathy is generally defined as loss of magnitude of renal artery stenosis has no direct correla-
renal function related to hypoperfusion from renal ar- tion with the severity of kidney disease, unless the
tery disease.23 Atherosclerotic renal artery disease affect- artery is completely occluded.25,26
ing both renal arteries or the artery to a solitary kidney Atherosclerosis is responsible for at least two thirds of
is a common cause of ischemic nephropathy. Bilateral cases of clinically significant renal artery stenosis.21 Ob-
occlusions may eventually cause end-stage kidney dis- struction usually results from aortic plaque engulfing
ease. However, diminished central blood flow may be a the renal artery ostium (i.e., within 5 to 10 mm of the
10. RENAL ARTERIES AND VEINS 293
aortic lumen). Less frequently, plaque develops inde- ease (about 25%), coronary artery disease, peripheral
pendently in the truncal portion of the renal artery. In arterial disease, and stroke.31
several studies, atherosclerotic renal artery stenosis was
found to be progressive in more than one third of Imaging
cases.27,28 However, conversion to frank thrombosis is Because hypertension is common but RVH is not, screen-
uncommon. Atherosclerotic renal artery disease must be ing should be reserved for patients at moderate to high
distinguished from other causes of renal artery obstruc- risk for RVH. Box 10-2 lists the criteria proposed by the
tion, particularly fibromuscular dysplasia (FMD; see later) Joint National Committee on Prevention, Detection,
(Box 10-1). Other kidney-related conditions that occa- Evaluation, and Treatment of High Blood Pressure.32
sionally lead to chronic hypertension include trauma Revised guidelines are currently in preparation.
(e.g., Page kidney), cystic disease, renal cell carcinoma Several metabolic screening tests may be first per-
(RCC) or pheochromocytoma, renal artery aneurysm, formed to exclude other uncommon causes of hyperten-
reninoma, and renal infarction. sion (e.g., pheochromocytoma, aldosteronoma). Nonin-
vasive imaging procedures are then used to further
Clinical Features screen patients. Catheter arteriography is employed
Most patients with atherosclerotic RVH or ischemic only when results are equivocal or endovascular ther-
nephropathy are middle aged or older adults and have apy is being considered. No single screening procedure
one or more risk factors for atherosclerosis. Younger has emerged as the ideal technique.
patients are more likely to suffer from one of the less
common causes of RVH (see later discussion). Although COLOR DOPPLER SONOGRAPHY
African Americans suffer from essential hypertension Ultrasound is one of the principal tools for detecting
more frequently than do whites, RVH is relatively more RVH because it is quick, relatively inexpensive, and
common in whites.29 Patients with thrombosis superim- completely safe (Fig. 10-13). If the aorta and main renal
posed on underlying disease often are asymptomatic. artery can be imaged, criteria for significant renal artery
However, worsening of hypertension or loss of renal stenosis include intrastenotic peak systolic velocity
function may occur when there is occlusion of the artery (PSV) of greater than 180 cm/sec and PSV renal/aortic
to a solitary functioning kidney. ratio of greater than 3.0 to 3.533,34 (Fig. 10-14). If these
In the United States, the prevalence of significant re- vessels cannot be seen because of technical factors, the
novascular disease (detected by duplex sonography) intrarenal arteries are interrogated. With significant re-
among individuals older than 65 years is about 7%.30 nal artery stenosis, damping and slowing of the time to
Significant atherosclerotic renal artery stenosis is associ- peak systole (parvus et tardus waveform) is typical.35
ated with particularly high rates of chronic kidney dis- In addition, flow acceleration is diminished and the ac-
celeration time prolonged (!300 to 390 cm/sec2 and
"0.06 to 0.07 sec, respectively).33,36 The resistive index
BOX 10-1
C AU S E S O F R E N A L A R T E R Y BOX 10-2
STENOSIS
S I G N S O F R E N O VA S C U L A R
H Y P E RT E N S I O N
Atherosclerosis
Fibromuscular dysplasia
Onset of hypertension in patients !30 or "55 years
Dissection
of age
Vasculitis
Resistant hypertension (blood pressure "140/90 mm Hg
Takayasu arteritis
on appropriate triple drug therapy)
Radiation arteritis
Accelerated hypertension
Coarctation syndromes
Recurrent (flash) pulmonary edema
Neurofibromatosis
Renal failure of uncertain etiology
Congenital rubella
Abdominal bruit
Williams syndrome
Renal insufficiency after ACE or ARB therapy
Tuberous sclerosis
Significant extrarenal occlusive arterial disease
Midaortic syndrome
Trauma ACE, angiotensin-converting enzyme inhibitor; ARB,
Extrinsic compression angiotensin II receptor blocker
294 III. VISCERAL ARTERIES AND VEINS
A B C
D E F
FIGURE 10-14 Severe left renal artery stenosis. A, Color Doppler ultrasound shows high peak systolic velocity (417 cm/sec) in the
proximal renal artery. B, Spectral waveforms of intrarenal arteries depict the tardus et parvus waveform expected with a significant
upstream stenosis. C and D, Aortography defines the tight truncal renal artery stenosis (arrow). The left kidney is small. E, The lesion is
crossed with a guidewire, and a balloon expandable stent placed. F, Post-stent arteriography shows a widely patent lumen, but embolization
of atheroma or thrombus into lower pole vessels is evident.
10. RENAL ARTERIES AND VEINS 295
A B C
FIGURE 10-15 Tight ostial left renal artery stenosis. A, Magnetic resonance angiography depicts the lesion well (arrow). B, Catheter
arteriography confirms the stenosis, which was treated successfully with a balloon-expandable stent (C). Note slight extension of stent into
the aorta.
A B
C
296 III. VISCERAL ARTERIES AND VEINS
stenoses of accessory arteries in this population are studies clearly depict the renal artery ostia and identify
uncommon (!2%).46 all renal arteries. Narrowing of accessory renal arteries
Multidetector row CT angiography achieves compa- or intrarenal branches can cause RVH and should be
rable sensitivity and specificity to MR angiography in carefully sought; intrarenal stenoses are particularly
depicting renal artery stenosis39,40,44,47 (Fig. 10-17). Sixty- common in children with RVH (Figs. 10-19 and 10-20).
fourdetector row CT is almost equivalent to catheter Stenoses may go undetected for several reasons, includ-
angiography in uncovering in-stent restenosis (which is ing oblique origin of the renal artery from the aorta and
obscured in MR angiography).48 Its major disadvantage superimposition of intrarenal branches. Multiple angio-
is the need for iodinated contrast in a population at graphic views may be necessary to identify such hidden
increased risk for contrast nephropathy. lesions.
Atherosclerosis produces irregular narrowing of the
CAPTOPRIL RENAL SCINTIGRAPHY renal ostium or proximal renal artery (see Figs. 10-14
To a great extent, this functional rather than anatomic and 10-15). Bilateral disease is common, and infrarenal
imaging modality has fallen out of favor in routine aortic atherosclerosis usually is present. After a stenosis
evaluation of patients with suspected RVH.40,49 has been identified, its hemodynamic significance must
be proved by one of the following criteria21,52:
RENAL VEIN RENIN SAMPLING
Reduction in luminal diameter of greater
Normally, the ratio of renin activity in the renal vein
than 75%
versus the IVC is about 1.24.50 In a patient with RVH and
Systolic pressure gradient across stenosis in
two functioning kidneys, the affected kidney overpro-
the main renal artery greater than 10 to 20 mm
duces renin, and renin secretion from the contralateral
Hg or greater than 20% of aortic systolic
kidney is suppressed. Several criteria have been used to
pressure
diagnose RVH based on renal vein renin values, includ-
ing a renal vein renin ratio between the involved and A stenosis with a 50% to 75% reduction in the luminal
uninvolved kidney of greater than 1.5 and a ratio of diameter may be hemodynamically significant, but in
(renal reninIVC renin)/IVC renin of greater than 0.48 such cases, pressures should be measured.
(Vaughan formula).51 While renal vein renin sampling
was once a mainstay of RVH diagnosis, it is seldom used Treatment
by interventionalists (Fig. 10-18). Selection of patients with RVH or ischemic nephropathy
for endovascular or operative therapy is highly contro-
CATHETER ANGIOGRAPHY versial21,53 (Box 10-3). Recent improvements in anti-
Catheter angiography is still the gold standard for the hypertensive medications and routine lifelong treatment
diagnosis of RVH. Initial abdominal aortography may of this population with lipid-lowering statins and oral
not be necessary if high-quality CT or MR angiography antiplatelet agents may allow many people with RVH
and normal or mild renal insufficiency to be treated
medically. The mere presence of a significant renal ar-
tery stenosis does not by itself warrant treatment, be-
cause not all such patients will have a positive clinical
outcome from arterial recanalization. In addition, the
procedure itself may worsen renal function by contrast
nephropathy, atheroembolization, or, rarely, complete
vessel occlusion.
A B
C D E
FIGURE 10-18 Renal vein renin analysis in patient with severe uncontrolled hypertension. A and B, Abdominal aortography shows two
left renal arteries, the more inferior of which has an origin stenosis (arrow). The right kidney is very small, and there is only minimal flow
through a highly diseased artery (arrow, C). Right (D), lower pole left (E), and upper pole left (not shown) renal vein renins were obtained.
Markedly elevated levels from the right kidney prompted right nephrectomy. Blood pressure was then easily controlled.
the interventional community are skeptical of routine Box 10-3 lists the primary indications for intervention
application of this aggressive approach. in patients with atherosclerotic RVH or ischemic ne-
phropathy.21,59 Angioplasty alone is rarely employed in
PATIENT SELECTION In patients with hypertension, this setting, with the possible exception of focal truncal
renal artery revascularization is of no proven value for stenoses.60 Stents significantly improve the technical
the following: success of renal artery angioplasty for atherosclerotic
disease, particularly for ostial lesions (from 55% to 70%
Nonsignificant renal artery stenosis to more than 95%).56,60-65 This improvement alone may
Incidental finding of significant disease in the largely explain the better long-term patency rates associ-
absence of hypertension or renal insufficiency ated with stent placement. Use of stents in renal arteries
Significant renal artery stenosis with severe with nominal diameter of less than 5 mm usually is
bilateral nephrosclerosis that may be responsible avoided because of the relatively higher rates of clini-
for hypertension cally significant restenosis in this setting.66
298 III. VISCERAL ARTERIES AND VEINS
BOX 10-3
I N D I C AT I O N S F O R
E N D O VA S C U L A R
AT H E R O S C L E R O T I C R E N A L
A RT E RY T R E AT M E N T
Revascularization for renal salvage is considered in administration of N-acetyl cysteine and intravenous
patients with significant bilateral renal artery disease bicarbonate infusion (see Chapter 2 and Fig. 3-20). All
or disease in a solitary functioning kidney with some patients should receive aspirin (325 mg orally) or clop-
functional reserve. Even when the main renal artery idogrel (300 mg oral loading dose) beforehand. If there
is completely occluded, collateral circulation has of- are no contraindications, the former is continued for
ten developed over time to keep the kidney viable, the patients lifetime or the latter for at least 3 to
even up to 6 months or more after occlusion. There 6 months afterward. Parenteral platelet inhibition may
is usually no benefit to revascularizing a minimally be helpful in minimizing deleterious effects to the
functioning kidney. kidney from atheroemboli or contrast.67,68 Full antico-
agulation with heparin (or a direct thrombin inhibitor
TECHNIQUE (SEE FIG. 10-14) Most interventional- if heparin allergy history exists) is instituted before
ists continue the patients blood pressure medication crossing the obstructive lesion. An intraarterial dose
until the procedure is completed. The dose of iodinated of nitroglycerin (150 to 200 mg) may help prevent
contrast material should be kept to an absolute mini- guidewire or catheter-induced vasospasm.
mum. In patients with preexisting renal dysfunction, The diagnostic catheter is replaced with a 5- or 6-Fr
various measures are taken to protect the kidneys guiding sheath or catheter with distal curve appropri-
including use of carbon dioxide angiography and ate for the renal artery origin. Traditionally, the stenosis
A B
10. RENAL ARTERIES AND VEINS 299
was crossed with a floppy 0.035 guidewire, a 5-Fr damage branch vessels. In the event of vessel rupture,
catheter advanced beyond the lesion, and the balloon an angioplasty balloon of appropriate size is quickly
or stent inserted over a stiff 0.035 Rosen or TAD ex- reinflated within the stent. Placement of a covered stent
change wire. Most practitioners now favor low-profile is usually required. The procedure ends with a com-
platforms.69 Thus the stenosis is crossed with a steer- pletion angiogram and pressure measurements to doc-
able 0.014 to 0.018 microwire followed by a micro- ument satisfactory result.
catheter. If difficulty is encountered traversing the
lesion, several maneuvers should be tried. Changes RESULTS Success in renal artery revascularization
in the patients respiration can dramatically alter the for RVH is judged by blood pressure response, with
aortorenal artery angle. Stiffer (or sometimes less stiff) clinical benefit defined as cure (i.e., blood pressure lower
guidewires may be helpful. than 140/90 mm Hg without medication) or improvement
A heavy-duty microwire with a floppy tip is posi- (i.e., reduced number of medications required to main-
tioned to give support for the balloon-mounted stent tain blood pressure below 140/90 mm Hg or a 15-mm
delivery catheter but avoid damage to the distal renal Hg reduction in blood pressure on the same or reduced
artery branches. Monorail systems that circumvent the number of medications).22 In ischemic nephropathy,
need for a long exchange wire are popular. Great care clinical benefit is defined as reduction or stabilization in
must be taken with wire manipulations because even a serum creatinine or flattening of the renal dysfunction
small-caliber floppy-tipped nitinol wire can dissect the curve (1/creatinine versus time).
main vessel or perforate small renal artery branches, A widely patent artery can be created with a metallic
leading to occlusion or hemorrhage. stent in greater than 95% of cases.24,61,63,72,73 In atheroscle-
Recent data prove that endovascular renal proce- rotic RVH, actual cure of hypertension is achieved in less
dures reliably cause showers of atheroembolic parti- than 10% to 20% of individuals whether stents are used
cles into the distal vasculature.70,71 This embolic bur- or not. Blood pressure control is better in about 50% to
den may negate any positive effect expected from the 80% of patients. Based on historical series, angioplasty
intervention. Distal embolic protective devices (occlu- and stent placement lead to improvement or stabiliza-
sion balloons or permeable filters) that trap this mate- tion of renal insufficiency in about 70% of cases; how-
rial may prevent microembolic injury to the treated ever, in some (but not all) series, that benefit diminished
kidney. These filters are strongly advocated by some over time.64,66,72,74 The value of embolic protection is
experts. unproven despite some encouraging nonrandomized
If the lumen is initially so narrow that passage of the series.67,68,75
guiding sheath or stent device is impossible, predilation The reported angiographic restenosis rate for athero-
of the stenosis with an undersized balloon may be re- sclerotic lesions is about 20%.63,66,76,77 However, the
quired. Off-label use of a variety of stents is standard reported Doppler sonographic restenosis rate at 9 to
practice but is not condoned by the U.S. Food and Drug 12 months has ranged from 21% to 50%.78,79 Luminal
Administration. The device is usually a nitinol stent that compromise seems to increase slowly over time. One
is factory-mounted on a slightly oversized diameter an- important predictor of clinically significant restenosis is
gioplasty balloon. It is chosen by measuring the luminal small initial vessel diameter (!5 mm). Preliminary trials
diameter of the normal portion of the renal artery suggest that drug-eluting stents may be of added value
or contralateral artery on the diagnostic arteriogram. in such small caliber arteries.80,81 Restenosis is treated by
In adults, the usual balloon diameter is 5 to 7 mm. The repeated balloon angioplasty without or with additional
shortest available stent length is selected to entirely stent placement82,83 (see Fig. 1-10).
cover the diseased area. The stent may be inserted into Despite encouraging results from retrospective stud-
the artery within the guiding sheath or directly over ies and registries, controlled randomized trials of stent
the guidewire without sheath protection (bareback). placement versus best medical therapy for patients with
The stent is exposed by withdrawing the guiding cath- atherosclerotic renal artery stenosis have not supported
eter from the renal artery. routine endovascular therapy for management of RVH
For ostial lesions, the stent is positioned with the or ischemic nephropathy.24,53,73,84,85 Critics are quick to
proximal end about 1 mm inside the aortic lumen to note the frequency of major adverse events associated
completely cover the overhanging plaque. Angiograms with stent insertion, including loss of renal function after
are obtained through the guiding sheath to ensure pre- revascularization in 10% to 20% of individuals.21 These
cise positioning. The stent is deployed by expansion of studies had numerous deficiencies, including inclusion
the balloon with an inflation device. Additional stents of a substantial number of patients with nonsignificant
are placed if needed, which is rare. Care should be renal artery stenosis and lack of standardization of stent
taken to avoid placing stents into the distal renal artery, insertion techniques. Nonetheless, the cumulative bur-
which could preclude later surgical revascularization or den of these recent trials is sobering. There is hope that
300 III. VISCERAL ARTERIES AND VEINS
the ongoing multicenter CORAL and RADAR trials will TABLE 10-2 Classification of Subtypes of Renal Artery
satisfy both proponents and skeptics of renal artery Fibromuscular Dysplasia
stent placement.87,88 Type Frequency (%) Morphology
A B
CATHETER ANGIOGRAPHY
BOX 10-4 Catheter arteriography is performed in the setting of
trauma or when endovascular therapy is being consid-
C AU S E S O F R E N A L A R T E R Y ered. An embolus appears as a filling defect or complete
OCCLUSION occlusion with concave margin (Fig. 10-23). Emboli tend to
lodge in the proximal renal artery or at a branch point.109
Thrombosis superimposed on underlying stenosis When embolization occurs into a normal vessel, the col-
Embolus (usually cardiac) lateral circulation may be inadequate to perfuse the kid-
Trauma ney. Embolization of intrarenal vessels leads to segmental
Accidental infarction. Traumatic occlusions usually produce an
Iatrogenic (e.g., catheterization) abrupt cutoff of the vessel at the site of injury (Fig. 10-24).
Aortic or renal artery aneurysm thrombosis
Dissection Treatment
Congenital (e.g., crossed fused ectopia) Although the native human kidney may only be viable
Vasculitis for several hours after sudden deprivation of blood
Thrombophilic state flow, renal revascularization following acute occlusion
Nephrotic syndrome has allowed salvage after much longer intervals.106,110,111
Collateral flow can preserve some kidney function for
weeks or even months after complete obstruction of a
previously normal vessel. Therefore treatment should
or penetrating abdominal trauma can produce an inti- not be withheld based solely on estimated time from
mal tear, dissection, or complete avulsion of the renal occlusion. Scintigraphy and sonography are sometimes
artery, any of which can result in acute thrombosis. Re- used to determine viability and residual mass.
nal artery dissection is usually an extension of the pro-
cess arising in the abdominal aorta. SURGICAL THERAPY
Most patients are older and have an underlying his- Renal artery thrombus is easily removed by surgical
tory of a heart condition, particularly atrial fibrillation or embolectomy. However, there is substantial morbidity
coronary artery disease. Individuals with acute occlu- and mortality associated with this procedure, mostly
sion of a previously patent renal artery may complain of related to patients existing cardiac diseases. Return of
sudden flank pain and hematuria. However, embolic renal function can be anticipated in some cases after
obstructions often are silent and may be missed for conservative treatment with anticoagulation and tempo-
some time. rary dialysis, as needed.112 Embolectomy is therefore
usually reserved for cases of bilateral embolism or
obstruction of a solitary kidney.
Imaging
CROSS-SECTIONAL IMAGING ENDOVASCULAR THERAPY
Color Doppler sonography is the simplest method for Although catheter-directed thrombolytic therapy can
detecting renal artery occlusion. If results are equivocal, completely dissolve most acute renal artery emboli,
CT or MR angiography should be performed.108 long-term kidney salvage is uncommon unless flow
A B
10. RENAL ARTERIES AND VEINS 303
A B
is restored within about 3 hours of occlusion113 (see ligated internal iliac artery is made. If the donor kidney
Fig. 10-23). Angioplasty and stent placement have been has multiple arteries, the accessory branches may be tied
effective in preserving function in some cases when individually into the main vessel. Sometimes, more
renal viability is proven.114 elaborate reconstruction is necessary.
Vascular complications develop in up to 25% of
Vascular Complications after Kidney patients after kidney transplantation.115 Arterial stenosis
Transplantation (Online Case 92) is the most common problem, encountered in about 4%
to 10% of transplant recipients.115-117 Most lesions
Etiology develop between 3 months and 2 years after placement.
The harvested kidney is placed into either iliac fossa of The stenosis is usually located at the anastomosis and
the recipient. The donor renal vein is sutured to the na- less often in the recipient or graft artery. Inflow iliac ar-
tive external iliac vein in an end-to-side fashion or the tery obstructions unsuspected before surgery also may
internal iliac vein in an end-to-end fashion. The donor contribute to declining allograft function. Stenoses are
artery is connected in one of two ways. The surgeon may more common in cadaveric grafts than in organs from
construct an end-to-side anastomosis to the recipient living-related donors. Immune-related proliferative nar-
external (or common) iliac artery (Fig. 10-25). In cadav- rowing has been postulated as the cause of some cases of
eric transplants, an oval segment of aorta surrounding graft arterial stenosis.118
the donor artery (Carrel patch) may be incorporated. Arterial thrombosis usually is the result of operative
Otherwise, an end-to-end anastomosis to the recipients injury to the donor or recipient artery, kinking of the
A B
304 III. VISCERAL ARTERIES AND VEINS
arterial connection, underlying atherosclerosis, acute The classic signs of transplant RVT are swelling and
rejection, thrombophilic state, or hypotension. Fortu- tenderness of the graft and impaired renal function.
nately, the incidence of complete main renal artery Patients with renal artery aneurysms may develop a
thrombosis is less than 1%; thrombosis of accessory pulsatile mass over the graft. Self-limited hematuria
branches or segmental infarcts is more common.119 or small perigraft hematoma is common after percuta-
Transplant renal vein thrombosis (RVT) may be caused by neous biopsy. If bleeding is exuberant or persistent, or
intraoperative damage to the vein, hypotension, venous the patient shows evidence for substantial blood loss
compression by an extrinsic mass (e.g., lymphocele), (based on vital signs, drop in hemoglobin, or postbi-
extension of lower extremity thrombus into the iliac opsy imaging), an angiogram should be performed
veins, or graft infection. without delay.
After operation, many patients require percutane-
ous biopsy of kidney transplants to assess graft func- Imaging
tion, and large cores of cortical and medullary tissue Imaging is used to distinguish vascular, medical, and
are required for analysis. There is a nontrivial risk of urinary tract complications as the cause of allograft
vascular injury; the consequence may be significant dysfunction.
immediate arterial bleeding or delayed hemorrhage
from pseudoaneurysm or arteriovenous fistula (AVF) for- SONOGRAPHY
mation. Aneurysms or pseudoaneurysms may also Color or power Doppler sonography is the standard
follow graft infection or loss of integrity of the arterial tool for screening patients with suspected vascular com-
anastomosis. plications after renal transplantation.119-121 The criteria
for significant arterial stenosis include a PSV ratio of
Clinical Features 2:1 or more (stenosis versus adjacent normal segment),
The most common signs of transplant renal artery ob- color aliasing, and a PSV of greater than 2 m/sec. Spec-
struction are hypertension, worsening renal function, tral analysis of intrarenal vessels may show a marked
and a bruit heard over the allograft. Because elevated slowing of acceleration time as an indirect indicator of a
blood pressure is common after transplantation, only proximal stenosis (Fig. 10-26). Segmental infarcts appear
patients with severe or refractory hypertension are eval- as sharply defined regions of absent flow in small paren-
uated for treatable causes. In addition to arterial stenosis chymal vessels. Sonography is useful also in detecting
or occlusion, a decline in renal function after transplan- renal artery thrombosis, RVT, renal vein kinks, AVFs,
tation may be caused by acute or chronic rejection, acute and pseudoaneurysms (Fig. 10-27). On color Doppler
tubular necrosis, drug reaction from immunosuppres- analysis, the pseudoaneurysm sac is often identified.
sive agents, or the development of intrinsic disease in AVFs show venous turbulence throughout the cardiac
the transplant. cycle.
A B C
FIGURE 10-26 Transplant renal artery stenosis. A, Color Doppler ultrasound of distal arterial system shows typical parvus et tardus
waveform because of upstream stenosis. B, Steep oblique left external iliac arteriogram barely documents the anastomotic stenosis (arrow).
C, After balloon angioplasty, vessel patency is markedly improved.
10. RENAL ARTERIES AND VEINS 305
A B
FIGURE 10-27 Transplant renal vein kink. A, Duplex sonography demonstrates markedly increased velocity and turbulence at the renal
vein anastomosis. B, Selective catheter venogram confirms tight narrowing because of a kink in the vessel.
COMPUTED TOMOGRAPHY AND MAGNETIC or long reverse-curve catheter from the contralateral
RESONANCE ANGIOGRAPHY groin. The renal vein may be approached from the ipsi-
In the typical setting of underlying renal graft insuffi- lateral groin. Care must be taken to strictly limit the
ciency, the great concern with contrast-based CT or MR volume of iodinated contrast material. The risk of con-
angiography is the associated risks of contrast nephrop- trast nephropathy is completely eliminated when car-
athy or nephrogenic systemic fibrosis, respectively. bon dioxide is used as the contrast agent.127 Steep oblique
Nonetheless, these modalities are often employed before projections often are required to lay out the arterial anas-
catheter angiography or surgical repair.121-124 Recently, tomosis (see Fig. 10-26). However, a single pressure
promising work in this arena has been reported with gradient across the anastomosis is far more accurate
steady-state free precision (SSFP) MR angiography that than multiple images for excluding a hemodynamically
totally avoids the risks of contrast materials.125 significant obstruction.
Arterial stenoses usually occur directly at the anasto-
CATHETER ANGIOGRAPHY mosis and produce little change in renal blood flow (see
Catheter arteriography and venography remain the gold Fig. 10-26). Other possible findings include iliac artery
standards for diagnosis. Given reported false-negative stenosis, segmental artery occlusion, main transplant
rates up to 14% and 18% for MR angiography and color artery stenosis, and vessel kink. Acute or chronic rejec-
Doppler sonography, respectively, in detection of trans- tion causes markedly diminished flow (!5 to 6 mL/sec),
plant renal artery stenosis, arteriography should be severe pruning of distal intrarenal branches, and a faint
pursued when clinical suspicion for vascular disease or absent nephrogram (Fig. 10-28). Renal artery or vein
remains high.126 Grafts with end-to-side anastomoses to thrombosis appears as complete or near-complete occlu-
the external iliac artery are best approached with a cobra sion of the vessel. Venous kinks also have been described
or hockey stickshaped catheter from the ipsilateral (see Fig. 10-27). AVFs and pseudoaneurysms have a
femoral artery. Grafts with end-to-end anastomoses to characteristic appearance and are virtually always intra-
the internal iliac artery usually are studied with a cobra renal (see later discussion).
306 III. VISCERAL ARTERIES AND VEINS
SURGICAL THERAPY
Operative treatment of arterial stenoses usually is re-
served for patients with a poor response to balloon
angioplasty or stenting. Surgical thrombectomy and
revision may be performed for cases of acute arterial
or venous thrombosis, although long-term salvage is
uncommon.
Grade Description
CATHETER ANGIOGRAPHY
Catheter angiography is reserved for the following FIGURE 10-29 Postnephrostomy renal artery pseudoaneurysm.
situations: Coronal T2-weighted magnetic resonance image shows a round mass
in the left renal pelvis with swirling flow, indicating an aneurysm.
Hematuria with hypotension or falling hematocrit
Persistent or recurrent hematuria
Hypotension or hypertension after documented
microcatheters are favored for embolization of both
renal injury
large and small arterial branches. In patients with AVFs,
Retroperitoneal hematoma detected by CT or
the coil should be large enough to avoid escape through
during surgery
the fistula into the venous system.145 Stents are placed
An initial abdominal aortogram will identify ac- to tack down post-traumatic renal artery intimal flaps
cessory renal arteries or suggest other sites of injury and avoid thrombosis or distal embolization146 (see
(e.g., bleeding from a lumbar artery). Angiographic Fig. 10-32).
findings vary widely and may include AVF, pseudo- Postembolization syndrome (fever, flank pain) is seen
aneurysm, frank extravasation, perirenal or retroperi- in a few patients. Nontarget embolization (usually of
toneal hematoma, intimal injury or dissection, or com- uninvolved renal vessels) is uncommon. Postemboliza-
plete renal artery occlusion (Figs. 10-31 and 10-32; see tion hypertension is unusual and usually transient.
Fig. 10-30).
Neoplasms (Online Cases 57 and 83)
Treatment Etiology
ENDOVASCULAR THERAPY The major benign and malignant neoplasms of the
Surgery, which almost always leads to unnecessary kidney are outlined in Box 10-5. Renal cell carcinoma
parenchymal damage, is reserved only for cases that (RCC) is the most common malignant neoplasm of the
cannot be treated by endovascular means.136,137,142 As a kidney.147,148 The most frequent subtype of RCC is clear
rule, grade I-III injuries are observed, grade V injuries cell, followed by papillary and chromophobe carcino-
deserve operative management, and many grade IV in- mas. Clear cell RCC is often encapsulated and ex-
juries are ideal for embolotherapy. Major CT findings tremely vascular. Tumor growth into the renal vein or
that suggest the need for intervention include large peri- IVC is characteristic but relatively uncommon (5% to
renal hematoma, frank arterial extravasation of contrast, 10% of patients).149,150 Recent investigations have iden-
and medial kidney laceration.143,144 To minimize tissue tified mutations in the von Hippel-Lindau (VHL) gene
loss, the embolic agent should be placed as close to the on chromosome 3 as the underlying defect in many
bleeding vessel as possible (see Figs. 10-30 and 10-31). sporadic and familial cases of clear cell RCC.151,152
Gelfoam pieces and microcoils placed through coaxial Gene dysfunction leads to accumulation of factors that
308 III. VISCERAL ARTERIES AND VEINS
C D
promote overproduction of tumorigenic vascular en- lipid, and connective tissue.157 Angiomyolipomas may
dothelial growth factors and platelet-derived growth be solitary or multiple and bilateral, as in patients with
factors. This discovery now explains the development tuberous sclerosis. Adenoma is a benign tumor of epithe-
of multiple, bilateral tumors in about 40% of patients lial cell origin. Oncocytoma is one form of adenoma that
with von Hippel-Lindau disease.153,154 Worldwide, the features cells with eosinophilic cytoplasm. The lesion
true incidence of RCC has been steadily growing over usually is solitary, well-defined, and often has a cen-
the past several decades; this development is only tral scar.158
partly explained by more frequent detection of inciden-
tal tumors in asymptomatic patients by cross-sectional Clinical Features
imaging.155 The classic symptom triad of malignant kidney tumors is
Wilms tumor is composed of a variety of cellular ele- hematuria, flank pain, and a palpable abdominal mass.147
ments and frequently produces areas of hemorrhage Rarely, patients may have hypertension directly related to
and necrosis.156 Angiomyolipoma (AML) is a renal ham- the tumor. Male patients with neoplastic invasion of the
artoma made up of blood vessels, smooth muscle cells, left renal vein may present with a left-sided varicocele.
10. RENAL ARTERIES AND VEINS 309
A B
However, many renal neoplasm are now discovered carcinoma features an enhancing mass in the renal pelvis
incidentally because of the widespread use of cross- or ureter. AML may be difficult to diagnose when small.
sectional imaging in medicine. Most people with malig- But when the tumor is large, the hallmark fatty compo-
nant kidney tumors are older than 50 years of age. RCC nent is distinctive (see Fig. 10-34). Assessing the extent of
affects men more frequently than women. On the other IVC thrombosis with RCC is crucial to operative planning.
hand, angiomyolipomas are commonly seen in middle- The Nevus classification stratifies cases with tumor throm-
aged women. Tumors associated with tuberous sclerosis bus less than 2 cm above the renal veins (level 1), below
tend to be more aggressive. Larger tumors are more the most inferior hepatic vein (level 2), below the dia-
likely to bleed. Most patients with Wilms tumor are less phragm (level 3), or supradiaphragmatic (level 4).149,150
than 5 years old.
CATHETER ANGIOGRAPHY
In RCC, the typical angiographic features are neovascu-
Imaging
larity, hypervascularity, dilation of the main renal artery,
COMPUTED TOMOGRAPHY AND MAGNETIC tumor stain, contrast puddling, displacement of normal
RESONANCE IMAGING renal vessels, and arteriovenous shunts with early ve-
Diagnosis and staging of benign and malignant renal neo- nous drainage160 (see Fig. 10-33). Parasitization of neigh-
plasms is accomplished with CT or MRI158,159 (Figs. 10-33 boring vessels (e.g., inferior mesenteric or lumbar arter-
and 10-34, and see Fig. 1-29). Clear cell RCC appears as ies) is relatively common (Fig. 10-35). Less than 10% of
an infiltrating or exophytic hypervascular mass with tumors are hypovascular, and most of these are of the
heterogeneity affected by cystic degeneration, bleeding, papillary type. Invasion of tumor into the renal vein or
or necrosis. The presence of tumor in the renal vein or IVC is characteristic.161
IVC should be sought (see Fig. 10-33). Papillary RCC is In contrast, Wilms tumor usually is moderately vas-
encapsulated and relatively homogenous. Transitional cell cular. Arteriography shows displacement of normal
310 III. VISCERAL ARTERIES AND VEINS
B C
A B
C D E
FIGURE 10-33 Renal cell carcinoma invading the renal vein and inferior vena cava (IVC). A and B, Magnetic resonance images show a
huge heterogeneous mass largely replacing the upper right kidney. There is invasion of the right renal vein and IVC, which is massively
enlarged (arrow). C and D, Renal arteriography shows a large mass with bizarre vascularity and numerous amorphous contrast lakes. The
deformity in the renal vein (arrows) represents tumor thrombus. E, After preoperative embolization with small microspheres, there is stasis of
flow in the renal artery.
ENDOVASCULAR THERAPY distal renal artery beyond adrenal and ureteral branches
In patients with renal neoplasms, transcatheter emboli- to avoid reflux of alcohol into the aorta, which may have
zation is requested for the following reasons165-167: disastrous consequences. The volume of alcohol can be
estimated by measuring the amount of contrast required
Devascularization before open or laparoscopic ne-
to fill the renal artery and branches with the occlusion
phrectomy to ease resection, minimize blood loss,
balloon inflated. Alcohol is slowly injected in small ali-
and possibly heighten the immune response
quots (1 to 5 mL) into the main renal artery. The balloon
against the tumor
is kept inflated for several minutes after injection and is
Palliative treatment in patients with unresectable
then slowly deflated. Patients commonly experience a
disease
profound postembolization syndrome, characterized by
Treatment or prevention of hemorrhagic compli-
fever, flank pain, and nausea. For microsphere ablation,
cations
microcatheters are used and small particles (e.g., 300- to
For RCC, the preoperative procedure usually is per- 500-micron microspheres) are preferred. Accessory or para-
formed within 24 hours of nephrectomy (see Figs. 10-33 sitized arteries may be treated in a similar fashion if there
and 10-35). However, it is important to realize that the is virtually no chance of nontarget embolization.
clinical benefits of this maneuver have not been rigorously For patients with AMLs, embolization has emerged
proven in controlled trials, and urologists are divided on as a useful alternative to surgery, particularly for symp-
the value of this approach.165,166,168-170 The most popular tomatic lesions and silent tumors larger than 4 cm (which
embolic agents are absolute ethanol and microspheres. For have a propensity to growth and hemorrhage).163,167,171-175
ethanol ablation, an occlusion balloon is advanced into the Tumor shrinkage and pain relief occur in many (but not
312 III. VISCERAL ARTERIES AND VEINS
A B C
D E F
FIGURE 10-34 Angiomyolipoma. A and B, Axial and coronal reformatted contrast-enhanced computed tomography images show a
well-circumscribed largely exophytic mass arising from the upper pole of the right kidney (arrow). The mass is heterogeneous, but has some
very low density elements similar to fat. No other renal lesions were identified. C, Right renal arteriography shows the hypervascular mass.
D and E, Superselective arteriography of the segmental branch feeding the tumor highlights its hypervascular, well-circumscribed nature.
F, After infusion of 300- to 500-micron Embospheres, the tumors blood supply is obliterated.
all) cases (see Fig. 10-34). Patients with smaller tumors procedures are offered to patients with bilateral tumors,
should be imaged periodically to assess growth. malignancy in a solitary kidney, and angiomyolipomas.147
A B
C D
FIGURE 10-35 Renal cell carcinoma parasitizing the right testicular artery. A, Abdominal aortography shows the markedly hypervascular
tumor. B, Following embolization of the distal artery, there is stasis of flow to the kidney, but the proximal superior capsular branch was
spared (arrow). C, Selective right testicular arteriography shows a markedly dilated vessel with supply to the mass. D, The artery was
embolized proximal to the mass with coils and Gelfoam.
branches around the dilated collecting system. Late-stage atherosclerotic changes (e.g., calcification) in some
chronic kidney disease causes the kidneys to shrink. Flow dysplastic aneurysms are probably a secondary effect
into the renal branches is markedly diminished, but the rather than causative. Dysplastic aneurysms typically
central artery usually remains patent. target the vessel segment near or just beyond the first
bifurcation of the main renal artery182 (Fig. 10-38).
These lesions are more frequent on the right side and
OTHER DISORDERS may be multiple or bilateral. Extrarenal pseudoaneu-
rysms usually are caused by trauma or infection.183
Intrarenal aneurysms are most commonly caused by
Aneurysms (Online Case 110) a penetrating trauma, necrotizing arteritis (e.g., poly-
Extrarenal artery aneurysms are most commonly arteritis nodosa), or illicit drug use (e.g., cocaine,
caused by arterial dysplasia, FMD, arteritis, trauma, methamphetamines), or are associated with tumors
infection, or a congenital abnormality (Box 10-6). The such as AML.184
314 III. VISCERAL ARTERIES AND VEINS
C B
10. RENAL ARTERIES AND VEINS 315
A B
316 III. VISCERAL ARTERIES AND VEINS
A B C
FIGURE 10-39 Bilateral renal artery aneurysms with rupture during pregnancy. A, Reformatted coronal computed tomography scan
shows massive acute retroperitoneal hemorrhage displacing the left kidney superiorly. B, Emergent aortography revealed a large left renal
artery aneurysm (small arrow) and incidental small right renal artery aneurysm (large arrow). Small caliber of all arteries reflects shock. C, The
left renal artery was quickly embolized to prevent further bleeding.
BOX 10-7
C AU S E S O F R E N A L A RT E RY
DISSECTION
A B
FIGURE 10-41 Renal artery dissection from extension of abdominal aortic dissection. A, Contrast-enhanced computed tomography shows
a geographic zone of hypoperfusion of the dorsal side of the right kidney as well as a dissection flap in the aorta (arrow). B, Aortography
through the true lumen shows poor filling of the right renal artery (large arrow) but good flow in the left renal artery (small arrow).
C D
318 III. VISCERAL ARTERIES AND VEINS
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C H A P T E R
11
Mesenteric Arteries
Karim Valji
ARTERIOGRAPHY
(ONLINE VIDEOS 11-1 TO 11-3)
ANATOMY C D
(ONLINE CASES 6 AND 19) FIGURE 11-2 Embryologic development of the mesenteric arteries
(right lateral view). A, In the fetus, the dorsal aorta on the left and the
ventral anastomotic channel on the right are connected by a series of
Development vitelline arteries. B, Normal anatomy at birth. C, Failure of a portion
In the fetus, a series of vitelline arteries arising from the of the ventral anastomosis to regress causes the hepatic artery to be
replaced to the superior mesenteric artery. D, Failed regression of
fused dorsal aortae supply the abdominal viscera.1
a segment of the ventral anastomosis between the celiac and superior
These branches are initially connected by a ventral mesenteric arteries leaves a direct collateral pathway (i.e., arc of
anastomotic channel (Fig. 11-2). The celiac, superior Buehler). (Adapted from Reuter SR, Redman HC, Cho KJ: Gastrointestinal
mesenteric, and inferior mesenteric arteries originate angiography. 3rd ed. Philadelphia: WB Saunders; 1986: p. 34.)
325
326 III. VISCERAL ARTERIES AND VEINS
from three of these vitelline segments; the remaining proper hepatic artery, which itself divides into right and
segments regress before birth. Common variants in left (and occasionally middle) hepatic arteries. Hepatic
mesenteric artery anatomy can be explained by abnor- arterial anatomy is detailed in Chapter 12. The right gas-
mal persistence of vitelline remnants or portions of the tric artery usually takes off from the proper or left he-
ventral anastomosis. patic artery but sometimes is not visualized on nonselec-
tive angiograms. It supplies the pylorus and the lesser
curvature of the stomach and communicates with distal
Normal Anatomy
branches of the LGA. The cystic artery usually originates
The celiac artery exits the anterior surface of the aorta at from the right hepatic artery, although it may arise more
about the T12 level2-4 (Fig. 11-3). The main trunk can take proximally.
an upward, downward, or forward course. Just beyond The GDA runs between the neck of the pancreas
its origin, the celiac artery gives off the LGA and then and the duodenum. Its first major branch is the poste-
divides into the common hepatic and splenic arteries. rior superior pancreaticoduodenal artery. This vessel
Sometimes, the inferior phrenic or dorsal pancreatic gives off branches to the pancreas on the left and to
artery arises directly from the celiac trunk. the duodenum on the right. The GDA then divides
The common hepatic artery runs toward the liver. After into its terminal branches, the anterior superior pancre-
giving off the gastroduodenal artery (GDA), it becomes the aticoduodenal artery and the right gastroepiploic artery.
Left gastric
Gastroduodenal artery
artery
Splenic
Common artery
hepatic
artery
B
FIGURE 11-3 Celiac arteriogram. A, Arterial phase. B, Venous phase with filling of the splenic and portal veins.
11. MESENTERIC ARTERIES 327
The superior pancreaticoduodenal arteries lead into mesenteric artery (SMA). The right gastroepiploic
an arterial network that supplies the head of the pan- artery runs along the greater curvature of the stomach
creas. These vessels have rich anastomoses with the and communicates with the left gastroepiploic branch of
corresponding branches of the inferior pancreatico- the splenic artery.
duodenal artery, which originates from the superior The splenic artery supplies the spleen, pancreas, and
stomach (see Chapter 12). It runs dorsal to the upper
border of the pancreas along with the splenic vein. Its
branches usually include the dorsal pancreatic, pancreatica
magna, short gastric, and polar arteries. The splenic artery
divides into superior and inferior branches near the
splenic hilum. The inferior polar artery gives rise to the
left gastroepiploic artery, which courses along the greater
curvature of the stomach.
The LGA exits the upper surface of the celiac artery
and runs toward the cardia of the stomach (Fig. 11-4).
At this point, it divides into several branches that supply
the distal esophagus and fundus of the stomach. These
vessels communicate with short gastric branches of
the splenic artery, the right gastric artery, and the left
inferior phrenic artery.
The SMA supplies the bowel from the distal duode-
num to the mid-transverse colon (Fig. 11-5). It courses
behind the body of the pancreas and then enters the
root of the mesentery. The superior mesenteric vein runs
along the right side of the artery. The inferior pancre-
FIGURE 11-4 Left gastric arteriogram. aticoduodenal artery is the first branch of the SMA,
B C
328 III. VISCERAL ARTERIES AND VEINS
although it may arise in a common trunk with the first rectal (hemorrhoidal) artery, which divides into right
jejunal artery. It passes to the right and superiorly into and left branches that supply blood to the rectum.
the head of the pancreas, where it communicates with
the superior pancreaticoduodenal branches of the
GDA. A series of jejunal and ileal branches occupy
Variant Anatomy
most of the main trunk of the SMA. Usually, these ves- Anomalies in the origins of the central mesenteric ar-
sels fan out from the left upper quadrant to the right teries are rare, but anomalies in the branching patterns
lower quadrant. A system of elaborate arcades be- of the mesenteric arteries are common. It is vital to be
tween these branches feed the vasa recta that directly alert to potential variants when performing angio-
supply the wall of the bowel. The ileocolic artery is the graphic procedures. Table 11-1 outlines the important
terminal continuation of the SMA. It gives off branches variants formulated by the classic anatomic studies of
to the ileum, appendix, cecum, and right colon. The Michel and coworkers5,6 (Figs. 11-7 through 11-9; see
right and middle colic arteries arise separately or as a also Fig. 7-4). The reported frequencies vary somewhat
common trunk on the right side of the SMA. These in postmortem and angiographic studies.
vessels supply the ascending and transverse colon, A replaced hepatic artery exists when an entire he-
respectively. Small bowel branches of the SMA can be patic lobe is supplied by a vessel with an aberrant
differentiated from colonic branches by their more origin. An accessory hepatic artery exists when a portion
extensive arcade system and longer vasa recta (see of the affected lobe is supplied by a vessel with
Fig. 11-5). an aberrant origin. Accessory hepatic arteries supply
The IMA supplies the colon from its mid-transverse isolated hepatic segments and are not redundant arter-
segment to the rectum (Fig. 11-6). The vessel runs infe- ies. As a rule of thumb, a replaced or accessory hepatic
riorly for several centimeters and then gives off the left artery arises from the LGA in 20% of patients and from
colic artery. An ascending branch of this artery joins the the SMA in 20%.
middle colic branch of the SMA. Descending colic Other rare variants include common origin of the
(sigmoid) branches originate from the left colic artery and celiac artery and SMA (celiomesenteric trunk, Fig. 11-10),
distal IMA to supply the lower descending and sigmoid separate origin of one or more major celiac branches
colon. The terminal branch of the IMA is the superior from the aorta, and splenic artery arising from the SMA
(Figs. 11-11 and 11-12).
Collateral Circulation
The intestinal tract has an extensive collateral net-
work that prevents or limits bowel ischemia when cen-
tral arteries become obstructed. The more important
pathways6 are outlined in Table 11-2 and shown in
Figures 11-13 through 11-16. The different collateral
routes between the SMA and IMA are often confused.
Text continued on p.332
A B
FIGURE 11-7 A, Replaced right hepatic artery (arrow) to the superior mesenteric artery. B, No filling of the right hepatic branches is seen
on the celiac arteriogram.
A B
FIGURE 11-8 Replaced common hepatic artery. A, The common hepatic artery originates from the superior mesenteric artery. B, At celiac
angiography, only the left gastric and splenic arteries are seen.
A B
FIGURE 11-10 Common celiomesenteric trunk on mesenteric arteriography (A) and sagittal shaded surface display CT angiography (B).
A B
FIGURE 11-11 Right hepatic artery takes off directly from the aorta (A), separate from the celiac trunk (B). The dorsal pancreatic artery
(D), transverse pancreatic artery (T), and omental branches (O) are seen.
CELIAC AND SUPERIOR MESENTERIC ARTERIES SUPERIOR AND INFERIOR MESENTERIC ARTERIES
(SEE FIG. 11-13) (SEE FIG. 11-15)
Pancreatic arcade Gastroduodenal and inferior Marginal artery Branches of middle and left colic
pancreaticoduodenal arteries arteries (of Drummond)
Arc of Buehler Direct embryologic pathway Arc of Riolan Central vessel from middle to left
colic artery
INTRACELIAC BRANCHES (SEE FIG. 11-14)
INFERIOR MESENTERIC AND ILIAC
Gastric arcade Left and right gastric arteries
ARTERIES
Gastroepiploic arcade Left and right gastroepiploic arteries
Arc of Barkow Left and right epiploic arteries Rectal (hemorrhoidal) Superior and middle/inferior rectal
(within omentum) arteries arcade
B
FIGURE 11-15 Marginal artery of Drummond and arc of
FIGURE 11-14 Gastroepiploic arcade. The right gastroepiploic Riolan with inferior mesenteric artery (IMA) occlusion. A, Superior
artery (R), the terminal branch of the gastroduodenal artery (G), mesenteric arteriogram shows dilation of the middle colic artery
continues to the left gastroepiploic artery (L) in the splenic hilum. with flow into the IMA distribution (arrow). B, Selective middle colic
This pathway provides collateral circulation with splenic artery artery injection shows filling of the arc of Riolan (arrowhead) and the
obstruction. Also note the replaced right hepatic artery. marginal artery (open arrowhead).
332 III. VISCERAL ARTERIES AND VEINS
A B
on severe atherosclerotic disease near the origin of central mesenteric vessels. Findings on CT or MRI
the SMA. include bowel distention and wall thickening, edema of
Nonocclusive mesenteric ischemia is responsible for the mesentery, intramural gas, and, sometimes, dimin-
some cases of bowel ischemia.11-12 The disorder is caused ished bowel wall enhancement. Filling defects in the
by hypotension or hypovolemia in the setting of acute major mesenteric arteries and veins should be carefully
cardiac disease, sepsis, liver or kidney disease, and after sought (Figs. 11-17 and 11-18).
recent surgery. Certain drugs (including digitalis, dopa-
mine, and vasopressin) have also been implicated. CATHETER ANGIOGRAPHY
Regardless of the cause, the result is persistent vasocon- Arteriography is indicated when noninvasive imaging
striction of the SMA and its branches leading to intesti- is equivocal, nonocclusive mesenteric ischemia is sus-
nal hypoxia. This entity is particularly lethal; the 30-day pected, or endovascular treatment is contemplated.
mortality rate despite surgery in one large contempo- Arteriographic findings depend on the cause of occlu-
rary series was 80%.13 sive disease. A fresh embolus produces a discrete fill-
Superior mesenteric vein thrombosis may be spontane- ing defect (see Fig. 11-17). In some cases, residual flow
ous or secondary to portal hypertension, thrombophilic is seen around the clot. Reconstitution of the distal
states, trauma, abdominal surgery, inflammatory bowel SMA is usually poor or nonexistent. Occasionally,
disease, sepsis, neoplasm, or pancreatitis.14 If the venous small clots are seen in distal SMA branches or other
collateral circulation is inadequate, the bowel wall abdominal and pelvic arteries. Thrombotic occlusion
becomes edematous, and arterial inflow is diminished. causes complete obstruction in the most proximal por-
Finally, extension of an aortic dissection into main mes- tion of the SMA trunk (see Fig. 11-16). Because throm-
enteric trunks is an important reason for inadequate bosis usually occurs at a site of previous narrowing, the
perfusion of bowel. collateral circulation is often well developed. Despite
certain distinguishing features, it may be impossible
to differentiate thrombotic and embolic occlusions by
Clinical Features angiography.
Most individuals with acute mesenteric ischemia are Nonocclusive mesenteric ischemia is characterized by
older adults. Many have associated conditions such slow flow in the SMA, diffuse narrowing of SMA
as congestive heart failure, coronary artery disease, val- branches and arcades, segments of alternating spasm
vular heart disease, dysrhythmias, or hypotension. and dilation of these branches, and poor filling of the
Patients usually present with acute onset of moderate vasa recta11,22 (Fig. 11-19). Contrast persists in intestinal
to severe abdominal pain, sometimes accompanied by branches for greater than 2 seconds after the injection
nausea and vomiting or gastrointestinal bleeding. Clas- has ended. Profound systemic hypotension (shock
sically, the symptoms are out of proportion to the rela- bowel) and certain vasoconstricting drugs can produce
tively benign findings on physical examination. Often, a similar findings (see later discussion).
leukocytosis and metabolic acidosis are present. If bowel Superior mesenteric vein thrombosis is diagnosed by
infarction occurs, signs of an acute abdominal condition the presence of numerous collateral channels in place
will develop. Prompt diagnosis is important to avoid of the superior mesenteric vein during the late-phase
irreversible bowel damage, perforation, and sepsis, SMA arteriogram. Sometimes a filling defect in the
which usually occurs within 12 to 24 hours of occlusion main trunk of the vein is seen. Venous obstruction is
unless the collateral circulation is already well devel- usually associated with slow flow in the SMA and slow
oped. If the condition is left untreated, the mortality rate washout of mesenteric branches. However, chronic
can be as high as 60% to 100%.15,16 mesenteric artery or vein occlusion may be an inciden-
tal finding in patients with acute abdominal pain from
Imaging other causes.
Patients with a high likelihood of acute ischemia and
evidence of peritonitis or shock often undergo immedi-
Treatment
ate operation without undergoing a complex imaging
workup. SURGICAL THERAPY
Acute SMA occlusion is treated by embolectomy, throm-
CROSS-SECTIONAL TECHNIQUES boendarterectomy, patch angioplasty, or bypass graft-
Duplex ultrasound, computed tomography (CT), and ing along with resection of infarcted bowel.7,8 Many
magnetic resonance imaging (MRI) can play an impor- patients still require a second look operation to iden-
tant role in diagnosis and are particularly useful for tify additional ischemic bowel that must be removed.
excluding other sources of abdominal pain.17-21 Sono- Despite early and aggressive treatment, 30-day mortality
graphy is used primarily to assess the patency of the is still close to 30%.23,24
334 III. VISCERAL ARTERIES AND VEINS
A B
C D
FIGURE 11-17 Embolus to the superior mesenteric artery (SMA). A and B, Contrast-enhanced computed tomography scan shows
filling defect in proximal SMA trunk (arrow). Also note multiple loops of very dilated, fluid-filled small bowel with possible gas in the wall.
C, SMA angiography reveals the nonocclusive SMA embolus with extension into at least one jejunal branch (arrow). D, Following overnight
thrombolysis with t-PA at 1 mg/hr, there is near complete resolution of clot. Patients symptoms resolved.
BOX 11-2
C AU S E S O F C H R O N I C
MESENTERIC ISCHEMIA FIGURE 11-19 Nonocclusive mesenteric ischemia. There is
slow flow in the superior mesenteric artery (SMA), constriction of
intestinal branches, and alternating segments of dilation and
Atherosclerosis narrowing in the distal SMA (arrow).
Thrombotic occlusion
Celiac artery compression (median arcuate
the fasting state, respectively29-31 (Fig. 11-20). CT or MR
ligament) syndrome
angiography more thoroughly depicts mesenteric vascular
Dissection
stenoses and occlusions17,18 (Fig. 11-21). It is commonly
Extrinsic compression
accepted that at least two of the three mesenteric arteries
Vasculitis
must have significant stenoses or occlusions to make the
Tumor
diagnosis of chronic mesenteric ischemia. On the other
Inflammatory mass
hand, the mere presence of severe multivessel mesenteric
Coarctation syndromes
artery disease can be an incidental finding in a patient with
Vasoconstricting drugs
other causes for abdominal pain.
Fibromuscular dysplasia
CATHETER ANGIOGRAPHY
Arteriography is usually a prelude to percutaneous or
patients have diarrhea, nausea, or intermittent vomiting. open repair. Several entities should be considered in the
The abdominal examination is usually unimpressive, differential diagnosis of mesenteric artery narrowing
although an epigastric bruit may be heard. (see Box 11-2). Because of the chronic nature of the
disease, the collateral circulation is usually extensive.
Obstruction of the IMA is suggested by enlargement of
Imaging
the marginal artery (or arc of Riolan) with retrograde
CROSS-SECTIONAL TECHNIQUES flow into the IMA trunk (see Fig. 11-15).
Because the symptoms of chronic mesenteric ischemia are
often vague and intermittent, the diagnosis is often de- Treatment
layed. Duplex sonography is the primary imaging tool for Revascularization is performed to relieve chronic ischemic
screening in suspected cases. Criteria for diagnosis include symptoms, prevent the development of life-threatening
major vessel occlusion, high-grade stenosis, or peak sys- acute mesenteric ischemia, or avoid postoperative
tolic velocities in the celiac and superior mesenteric arteries ischemia if the IMA is to be sacrificed during an aortic
of greater than 200 cm/sec and greater than 275 cm/sec in operation or intervention.
336 III. VISCERAL ARTERIES AND VEINS
A B
SURGICAL THERAPY
The most common procedures for mesenteric revascu-
larization are transaortic thromboendarterectomy, aorto-
visceral bypass, and arterial reimplantation.23,32
ENDOVASCULAR THERAPY
Balloon angioplasty with stenting of the celiac artery
and SMA is an acceptable alternative to surgery in some
cases, particularly when the patient is at high risk for
operative complications8,32-36 (Fig. 11-22). Technical suc-
cess is reported in 30% to 90% of cases. However, major
complications occur frequently (16% to 33%) in some
series.34 Surgery is more effective than endovascular re-
pair; it affords more durable results and requires fewer
reinterventions to maintain patency. Angioplasty and
stent insertion is not useful in patients with celiac artery
compression syndrome.
A B
FIGURE 11-22 Superior mesenteric artery (SMA) angioplasty and stent placement in a patient with an abdominal aortic aneurysm
and occlusion of the inferior mesenteric artery. A, The lateral aortogram shows a tight proximal SMA stenosis (arrow). B, After placement
of a stent mounted on a 6-mm angioplasty balloon using a brachial approach, the stenosis is relieved. The residual systolic pressure gradient
was 7 to 8 mm Hg.
Aortoenteric fistula occurs in less than 1% of patients the large bowel. About 10% of the time, apparent lower
after aortic graft placement. The fistula develops gastrointestinal bleeding is attributable to rapid hemor-
between the bowel (usually the transverse duode- rhage from an upper source.54,55
num) and the graft as a consequence of infection.47
Marginal ulcers occasionally complicate surgical Diverticular disease is sometimes complicated by
gastrojejunostomy.48 Ulcers are located on the hemorrhage. Bleeding is minor and stops spontane-
jejunal side of the anastomosis; however, bleeding ously in most cases. Massive or recurrent bleeding
may occur from branches of the celiac artery is an indication for angiography. Hemorrhage
or SMA. occurs from a branch of the vasa recta in continuity
Dieulafoy disease is a noninflammatory disorder in with the body of the diverticulum.56 Diverticula are
which a small superficial gastric mucosal erosion most common in the sigmoid and left colon. For
covers a submucosal artery and may result in several reasons, colonoscopy identifies more
bleeding.49,50 The lesion is usually found in the left-sided bleeding diverticula and angiography
cardia or fundus of the stomach, but is rarely seen more right-sided diverticula.52,53,56
in the colon or small bowel. Angiodysplasia (vascular ectasia) is a developmental
vascular anomaly consisting of clusters of dilated
Box 11-4 outlines the major causes of lower gastroin- submucosal veins and capillaries in the bowel wall,
testinal bleeding.51 Based on two large epidemiologic most frequently in the ascending colon.55 The cause
studies, the most common causes of lower gastrointesti- is unknown. There is speculation that intermittent
nal bleeding among inpatients are diverticular disease, elevation in intraluminal pressure causes venous
colitis, neoplasms and anorectal disorders.38,52,53 How- obstruction, which over time leads to venous
ever, in angiographic series the most common sources engorgement and bleeding. Lesions are often
are diverticulosis, angiodysplasia, and polyps or cancer multiple. Angiodysplasia is relatively common in
(spontaneous lesional hemorrhage or postendoscopic the elderly and may be an incidental finding in
biopsy). At least two thirds of cases are localized to patients with other sources for gastrointestinal
bleeding. Although bleeding usually stops spon-
taneously, rebleeding occurs in the majority of
untreated lesions.54
BOX 11-4 Acquired immunodeficiency syndrome can cause
lower or upper gastrointestinal hemorrhage.
C AU S E S O F A C U T E L O W E R A wide variety of lesions may bleed, including
GASTROINTESTINAL Kaposi sarcoma, lymphoma, and a host of
BLEEDING opportunistic infections.58
Meckel diverticulum is a congenital remnant of
Diverticular disease the fetal omphalomesenteric (vitelline) duct that
Angiodysplasia (vascular ectasia) is seen in about 2% of the general population.
Neoplasms (benign polyps or malignant tumor) The outpouching occurs about 2 feet proximal
Spontaneous to the ileocecal valve. Gastric or pancreatic mucosa
Bleeding after endoscopic biopsy or in the lesion may be detected by 99mTc scanning. It
polypectomy is a common cause for lower gastrointestinal
Anorectal disorders (hemorrhoids, fissures, bleeding in children.
radiation proctitis, trauma)
Inflammatory bowel disease Clinical Features
Ischemic bowel Upper gastrointestinal bleeding is much more common
Arteriovenous malformations or telangiectasia than lower tract hemorrhage, but interventionalists
Radiation enteritis encounter the latter more often. Patients with significant
Vasculitis upper gastrointestinal bleeding have bright red or coffee-
Colonic or small bowel varices ground hematemesis or melena. Patients with lower
AIDS-related conditions gastrointestinal bleeding present with hematochezia or
Ulcer melena. However, about 10% of individuals with major
Aortoenteric fistula upper gastrointestinal hemorrhage have hematochezia
Meckel diverticulum suggesting a lower tract source.55 At least 75% of pa-
tients with acute gastrointestinal bleeding respond
AIDS, acquired immunodeficiency syndrome
to supportive measures and minor blood transfusions
alone. The remainder require direct intervention.
11. MESENTERIC ARTERIES 339
Imaging RADIONUCLIDE SCANNING
After the patient is resuscitated, endoscopy or anoscopy Scintigraphy is most often done with 99mTc-labeled red
is usually performed to identify and possibly treat a blood cells.60,61 The threshold for detection of gastro-
culprit lesion. In most individuals, minor or moderate intestinal bleeding is quoted as ranging from 0.05 to
bleeding stops spontaneously. In a minority, a source 0.4 mL/min, compared with a rate of about 0.5 to
is actually found (and often treated) with endoscopy/ 1.0 mL/min with angiography.62-64 However, these fig-
colonoscopy. Contrary to popular teaching, colonoscopy ures are based on animal models, phantom studies, and
after rapid cleansing is often useful in patients with ac- estimated transfusion requirements and are only ap-
tive lower gastrointestinal bleeding.38,40,41 Radionuclide proximations. Criteria for a positive study include pro-
scans or CT angiography are appropriate for assessing gressive accumulation of activity corresponding to a
hemodynamically stable patients with moderate to se- segment of bowel and movement over time because
vere but intermittent bleeding. The scan may localize the of tracer transit60,61,65 (Fig. 11-23). One important advan-
hemorrhage and determine whether it is brisk enough to tage of red cell scintigraphy is the ability to detect inter-
be seen at catheter angiography. Patients with continuous mittent bleeding over a 24-hour period. Patients with a
rapid bleeding, transfusion of more than four to six units negative scan are observed. Patients with a positive scan
of packed red blood cells over 24 hours, or hemody- should go to an interventional suite immediately. Local-
namic instability should undergo angiography without ization by scintigraphy may guide arteriography but is
delay. sometimes misleading.66
A B
C D
FIGURE 11-23 Right colonic bleed. A, Scintigraphy with 99mTc-labeled red blood cells shows early uptake in the right upper quadrant,
which is consistent with hepatic flexure bleed (arrow). B, The superior mesenteric arteriogram shows extravasation from a branch of the right
colic artery (arrow). C, Coaxial microcatheter is advanced to the site of bleeding. D, After placement of several microcoils and small Gelfoam
pieces, bleeding has stopped.
340 III. VISCERAL ARTERIES AND VEINS
COMPUTED TOMOGRAPHY ANGIOGRAPHY of all these studies are negative, inferior mesenteric arte-
Recently, contrast enhanced CT has become a popular riography should be considered. Presumed lower gastro-
method for noninvasive localization of gastrointestinal intestinal bleeding requires both superior mesenteric and
bleeding67-71 (Fig. 11-24). The diagnosis requires the pres- inferior mesenteric arteriography. Some practitioners
ence of hyperattenuated contrast material (compared prefer to study the latter vessel first to minimize obscu-
with the noncontrast scans) within the bowel lumen. A ration by the contrast-filled bladder. If results of both
recent metaanalysis of published work calculated a studies are negative, celiac arteriography is warranted.
pooled mean sensitivity and specificity of 89% and 85%, Aortography is needed only when ostial disease or vari-
respectively, for CT angiography. In the future, this more ant anatomy makes catheterization difficult or when the
robust modality may entirely replace red cell scintigra- examiner is trying to find other aortic branches that may
phy in the imaging workup for this clinical situation. be the source of bleeding (e.g., inferior phrenic artery).
The entire length of bowel supplied by the injected artery
CATHETER ANGIOGRAPHY must be visualized by using careful patient positioning
Nusbaum and Baum72 pioneered the angiographic tech- and multiple angiographic runs. Selective injections are
nique for evaluating gastrointestinal hemorrhage. The used to confirm suspicious findings on nonselective an-
vessel most likely to supply the bleeding site (based giograms. Patients with suspected aortoenteric fistulas
on clinical scenario and results of endoscopy, scintigra- are studied by CT rather than angiography.
phy, or CT angiography) is studied first. Upper gastro- The hallmark of gastrointestinal hemorrhage is extrava-
intestinal bleeding is evaluated by celiac arteriography, sation of contrast material into the bowel (see Fig. 11-23).
followed by superior mesenteric arteriography. If no Occasionally, extravasated contrast has a curvilinear
bleeding site is found, selective left gastric or gastroduo- shape that mimics a vascular structure (pseudovein
denal arteriography may detect a subtle bleed. If results sign) (Fig. 11-25). Several entities can be confused with
A B C
D E F
FIGURE 11-24 Arteriovenous malformation of the jejunum. A and B, Arterial phase of computed tomography scan shows dense round
bumps on the wall of the jejunum (arrows). C, Superior mesenteric arteriography fails to show lesion prospectively. D and E, After sequential
interrogation of jejunal branches, the vascular malformation is identified. F, More selective injection reveals the extent of the lesion.
11. MESENTERIC ARTERIES 341
A B
FIGURE 11-27 Angiodysplasia of the cecum. A, Early phase of superior mesenteric arteriogram shows a tangle of vessels in the cecum
(arrow). B, Capillary phase exhibits early opacification of draining vein (arrow). Note that no venous drainage is seen from other portions
of the bowel.
natural hormone vasopressin (Pitressin) causes constric- However, with the development of coaxial microcath-
tion of smooth muscle of the bowel wall and splanchnic eters (which can be navigated directly to the site of
blood vessels. Infusion of the drug proximal to a bleeding bleeding) and newer embolic agents (e.g., microcoils),
mesenteric artery reduces blood flow, lowers the pulse the risk of significant bowel ischemia is now very
pressure, and allows a clot to form.80 Vasopressin is not low.86 Embolotherapy has the advantage of immediate
useful for bleeding directly from a large artery (e.g., gastro- and theoretically permanent control of bleeding with-
duodenal bleed, splenic artery pseudoaneurysm) or out the risks of vasopressin infusion or prolonged
at sites with dual blood supply (e.g., pyloroduodenal catheterization. For these reasons, the procedure has
bleeding). It is contraindicated in patients with severe become widely popular as first-line therapy for acute
coronary artery disease, dysrhythmias, or malignant gastrointestinal hemorrhage.86,87 Even in the absence
hypertension. of extravasation, empiric embolization of the LGA or
The catheter is placed in the central vessel feeding the GDA often is done to prevent recurrent bleeding in
bleeding site (celiac artery, LGA, SMA, or IMA). Vaso- patients with massive upper gastrointestinal bleeding
pressin is infused at 0.2 units per minute. After 20 to but negative angiograms88-91 (Fig. 11-28).
30 minutes, arteriography is repeated to look for resid- Embolotherapy is feasible because of the exten-
ual bleeding and the presence of some direct or collat- sive intestinal collateral circulation (particularly in
eral blood flow to the viscera (see Fig. 1-4). If bleeding the upper tract) through arterial arcades, communi-
has stopped, the infusion is continued while the patient cations between vasa recta, and submucosal inter-
is monitored in an intensive care unit. If bleeding per- connections. However, embolization is risky in the
sists, the infusion rate is increased to 0.3 or 0.4 units per setting of previous gastric or bowel surgery or radia-
minute, and arteriography is repeated 20 to 30 minutes tion therapy or when the collateral circulation is other-
later. If the lesion is still bleeding, alternate forms wise inadequate. 92
of therapy should be pursued. Vasopressin therapy is Acute hemorrhage from angiodysplasia or arte-
continued for 6 to 24 hours and then gradually tapered riovenous malformations may initially respond to
over 12 to 48 hours. embolotherapy.93,94 Contrary to popular wisdom,
Vasopressin therapy is initially very effective for cer- several recent series found that distal microemboli-
tain types of gastrointestinal hemorrhage, particularly zation provided relatively durable obstruction for
colonic diverticular and gastric mucosal hemorrhage. angiodysplasia in over 50% of cases.93-95 Still, bleed-
Initial success rates range from 60% to 90%.81-83 How- ing can recur, and those lesions should be removed
ever, rebleeding is the rule, and major adverse events are operatively. In the case of right-sided angiodysplasia,
reported in up to 20% of cases.84,85 a right hemicolectomy is performed to eliminate the
bleeding lesion and any other occult lesions. Small
EMBOLIZATION bowel arteriovenous malformations are notoriously
The goal of embolotherapy is to stop blood flow to the difficult to find at surgery. The involved segment of
bleeding artery while maintaining viability of the bowel is much easier to locate if a coil is deposited in
bowel. For many years, embolization, particularly a distal feeding branch or a coaxial microcatheter is
in the small intestine and colon, was avoided by angi- left in place for methylene blue injection during the
ographers because of the fear of bowel infarction. operation.96,97
11. MESENTERIC ARTERIES 343
A B C
D E F
FIGURE 11-28 Prophylactic embolization for a young woman with graft vs. host disease and failed endoscopic clipping of an upper
intestinal hemorrhage after duodenal biopsy. A, No active bleeding is seen on the celiac arteriogram. B, Superior mesenteric arteriography
reveals a replaced right hepatic artery (long arrow). A proximal branch (short arrow) was determined to be an anomalous pancreaticoduodenal
vessel (C). D, Microcoils were deposited to occlude this potential bleeding source. Then, the gastroduodenal artery was selectively engaged
with a microcatheter (E) and completely blocked with multiple microcoils (F). The patient did not bleed again.
TECHNIQUE A microcatheter is placed coaxially into levels. For example, after embolizing the GDA for a
the diagnostic catheter residing in the main trunk of the duodenal ulcer hemorrhage, a superior mesenteric arte-
primary mesenteric artery. A steerable microwire is nego- riogram is done to evaluate the inferior pancreatico-
tiated to the culprit arterial branch. It may be challenging duodenal supply to the duodenum. Embolization of
to pick out the particular branch that is bleeding, so se- the back door to the arcade may be necessary, although
quential injection into multiple vessels often is necessary. this increases the risk of ischemia102,103 (Fig. 11-32). Be-
The optimal site for depositing embolic material is now fore finishing the case, the proximal mesenteric artery is
established. Early teaching favored proximal occlusion.98 restudied to be certain there is no extravasation through
Experts now recommend more peripheral embolization collateral vessels.
just proximal to the vasa recta feeding the bleeding site
to minimize the length of bowel at risk for ischemia.86,87,99 RESULTS In contemporary series, embolotherapy
The most commonly used embolic agents are mi- successfully stops gastrointestinal bleeding in about
crocoils, Gelfoam pieces, microparticles and cyanoacry- 80% of patients.54,94,95,104-112 The primary reason for tech-
late (glue)100,101 (Figs. 11-29 through 11-31). Coils can be nical failure is inability to obtain proper microcatheter
delivered with precision and are permanent. Recanaliza- position.54 Recurrent hemorrhage (within 30 days of
tion seems to be more frequent when microcoils are used treatment) occurs in about 20% of cases (Box 11-5). Re-
alone.91 Both large and small PVA particles (threshold bleeding may be more frequent with inflammatory le-
300 "m) have been used safely by some groups. Material sions and arteriovenous malformations. If it occurs, re-
is deposited until the bleeding has stopped. peat angiography (and embolization) may improve
If a lesion is situated within an arcade fed by two success rates by identification of recanalized sites and
mesenteric arteries, angiography is performed at both new sources of bleeding (see Fig. 11-32).
344 III. VISCERAL ARTERIES AND VEINS
A B
C
11. MESENTERIC ARTERIES 345
A B
C
346 III. VISCERAL ARTERIES AND VEINS
A C
B
FIGURE 11-31 Duodenal hemorrhage after endoscopic sphincterotomy during endoscopic retrograde cholangiopancreatography.
A, Superior mesenteric arteriogram shows extravasation (arrow) from a duodenal branch of the first jejunal artery. B, A microcatheter
is advanced into the feeding vessel. C, After embolization, hemorrhage has stopped.
A B C
D E F
FIGURE 11-32 Recurrent upper gastrointestinal bleeding due to collateral arcade circulation. A, Initial gastroduodenal arteriogram shows
marked hypervascularity without frank extravasation. The feeding branches could not be selectively catheterized. B, Embolization
was performed across the gastroduodenal artery. C, Patient developed recurrent bleeding. Repeat gastroduodenal arteriography confirmed
persistent occlusion (not shown). Superior mesenteric arteriography is suspicious for bleeding from the inferior pancreaticoduodenal artery
(arrow). D, Selective catheterization confirms the bleeding. E, The first of two feeding vessels is selected up to the site of bleeding (arrow).
F, After embolization of both distal vessels, bleeding has stopped.
The SMA and IMA are usually patent in these patients, progressive expansion, rupture, or thrombosis. Stent
and the existing collateral circulation should be adequate graft placement is often employed when feasible.
to prevent intestinal ischemia. Nonetheless, symptoms Gastric, duodenal, or pancreaticoduodenal artery
have been attributed to visceral ischemia or to compres- pseudoaneurysm is a rare complication of an adjacent
sion of the celiac neural plexus. Surgical treatment, which inflammatory process (e.g., pancreatitis, peptic ulcer
may include division of the crus, release of sympathetic disease), trauma, or hyperdynamic state138 (Fig. 11-35).
nerve fibers, and revascularization, is often curative, Many of these patients present with gastrointestinal
although the results may not be durable.130,132 tract or intraabdominal bleeding and abdominal pain
(see Fig. 13-6). The growth rate is unpredictable, and
such aneurysms are often lethal without treatment. The
Aneurysms preferred therapy is transcatheter embolization.139,140
Aneurysms of the mesenteric arteries are uncommon.
Splenic and hepatic artery aneurysms, which are the
Vasculitis
most common splanchnic aneurysms, are considered in
Chapter 12. The very rare SMA and celiac artery aneu- Mesenteric arteritis is rare. A wide variety of small vessel
rysms (both true and false) are caused by atherosclerosis, vasculitides may cause nonspecific findings on CT and
a degenerative vasculopathy, infection, or trauma133-137 MR (segments of bowel wall thickening and enhance-
(Fig. 11-34). A few patients present with abdominal dis- ment, bowel distention, venous thrombosis) related to
comfort, but most are diagnosed incidentally on imaging inflammation, ulcerations, ischemia, and perforation.141,142
studies. The natural history of these aneurysms is that of These include Wegener granulomatosis, microscopic
348 III. VISCERAL ARTERIES AND VEINS
A B
FIGURE 11-33 Celiac artery compression in an asymptomatic patient. A, Transverse computed tomography image reveals impingement
of diaphragmatic crus on the superior aspect of the celiac artery origin (arrow). B, Gadolinium-enhanced magnetic resonance angiogram in
sagittal projection depicts proximal celiac artery stenosis (arrow).
polyangiitis, Henoch-Schnlein purpura, collagen vas- (see Fig. 11-24). Angiodysplasia (i.e., vascular ectasia)
cular diseases, and Behet syndrome. is an acquired anomaly of submucosal veins found
Takayasu arteritis is an inflammatory vasculitis of primarily in the ascending colon (see Fig. 11-27). Telan-
large- and medium-sized arteries143,144 (see Chapter 1). Ste- giectasias and angiomas are usually associated with con-
nosis or, rarely, complete occlusion of the mesenteric genital or hereditary syndromes, including hereditary
arteries associated with abdominal aortic narrowing hemorrhagic telangiectasia, Klippel-Trenaunay syn-
occurs in about 20% of cases. drome, and blue rubber nevus syndrome.148,149 In these
Polyarteritis nodosa (PAN) is a necrotizing vasculitis disorders, multiple, punctate hypervascular lesions are
that can affect distal branches of the mesenteric arteries, typically scattered throughout the bowel (Fig. 11-36).
producing multiple small saccular aneurysms.145 Some of In advanced cases, vascular tangles and arteriovenous
these patients present with abdominal pain, gastroin- shunting may be seen. Arteriovenous fistulas are ac-
testinal hemorrhage, or ischemia. Branches of the re- quired lesions that usually result from penetrating
nal, hepatic, splenic, and pancreatic arteries often are trauma.150
involved.
Radiation arteritis can develop after high-dose radia-
tion therapy for abdominal or pelvic malignancies. The
Trauma
condition may lead to irregular narrowing and occlu- Most injuries are caused by penetrating trauma, although
sion of mesenteric arteries and veins.146 SMA or superior mesenteric vein disruption can occur
Buerger disease is an occlusive vasculitis that pri- with blunt or decelerating trauma or catheterization
marily affects small vessels of the extremities (see Chapter procedures.151,152 Patients with penetrating trauma to the
1). However, mesenteric artery involvement has been central mesenteric arteries usually die before reaching
described.147 medical care. Those who survive present with massive
hemoperitoneum or mesenteric hematoma and usually
undergo emergency laparotomy without imaging evalua-
Arteriovenous Malformations
tion. Trauma may also lead to vascular occlusion, arterio-
Arteriovenous malformations are congenital lesions that venous fistula, or pseudoaneurysm (Fig. 11-37). Isolated
can occur at any site in the intestinal tract. They may mesenteric artery injuries have been successfully treated
cause chronic, intermittent gastrointestinal hemorrhage with embolotherapy.150,153
11. MESENTERIC ARTERIES 349
A B C
D E F
FIGURE 11-34 Dysplastic celiac artery aneurysm. A and B, Contrast-enhanced axial and shaded surface display sagittal reformatted
computed tomography images show a saccular aneurysm arising from the undersurface of the celiac artery (arrow). C, Lateral celiac
arteriogram displays the aneurysm (short arrow). Note origin of left gastric artery (LGA, long arrow) across from aneurysm. The LGA is
embolized first to prevent retrograde flow from pressurizing the aneurysm after a stent graft covers the aneurysm neck (D). The balloon
expandable covered stent is positioned across the aneurysm neck (E), and final arteriogram shows aneurysm exclusion (F).
Segmental Arterial Mediolysis and massive bleeding. Celiac artery branches are most com-
monly affected.156-158 Multiple lesions may be present.
Fibromuscular Dysplasia
Embolotherapy of affected vessels has been reported.159
These rare noninflammatory conditions may be re-
lated.154,155 Unlike classic fibromuscular dysplasia (which
is rarely seen in the mesenteric arteries [Fig. 11-38]), seg-
Coarctation Syndromes
mental arterial mediolysis primarily affects the visceral The abdominal coarctation syndromes are rare congenital
and coronary arteries. Pathologically, it is characterized disorders that can narrow the abdominal aorta and its
by patchy destruction of medial smooth muscles cells major branches (see Chapters 1 and 7). Abdominal coarc-
that are replaced by fibrin, collagen, and granulation tis- tation is seen in patients with neurofibromatosis, congeni-
sue. The weakened arterial wall is predisposed to aneu- tal rubella, Williams syndrome, and tuberous sclerosis.
rysm formation and spontaneous dissection (Fig. 11-39). Although renovascular hypertension from renal artery
In the abdomen, patients present with vessel rupture and stenoses is common, mesenteric ischemia is rare.
350 III. VISCERAL ARTERIES AND VEINS
B C
FIGURE 11-35 Pancreaticoduodenal artery aneurysms because of hyperdynamic flow from celiac artery occlusion. Axial (A), reformatted
sagittal (B), and shaded surface display (C) computed tomography angiograms show dilated aneurysms in the pancreaticoduodenal arcade
bed (arrows). The celiac artery is occluded, so flow in the arcade has markedly increased and caused aneurysm formation.
11. MESENTERIC ARTERIES 351
FIGURE 11-36 Multiple telangiectasias of the stomach (arrows) in a patient with hereditary hemorrhagic telangiectasia. Note the communi-
cation of the injected left gastric artery with the right gastric artery (single arrow).
A B
FIGURE 11-37 Superior mesenteric artery (SMA) root pseudoaneurysm from blunt trauma. Patient sent to interventional radiology
directly from emergent laparotomy because of uncontrollable hemorrhage. A, SMA angiography shows large pseudoaneurysm of SMA
root (arrow). B, A balloon was inflated to stop bleeding while the patient returned to the operating room.
352 III. VISCERAL ARTERIES AND VEINS
FIGURE 11-38 Fibromuscular dysplasia of the common hepatic, FIGURE 11-39 Probable segmental arterial mediolysis. A fusi-
left gastric, and proximal splenic arteries (short arrows.) Note accessory form aneurysm of the middle colic artery is identified (arrow). Also
left hepatic artery from the left gastric artery (long arrow). seen are multiple saccular aneurysms of branches of the replaced
right hepatic artery.
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tion and revascularization for complicated mesenteric pseudoan- 1999;10:509.
eurysms: a report of two cases and a literature review. J Vasc Surg 157. Lee SI, Chew FS. Splanchnic segmental arterial mediolysis. AJR
2007;45:381. Am J Roentgenol 1998;170:122.
138. Eckhauser FE, Stanley JC, Zelenock GB, et al. Gastroduodenal 158. Michael M, Widmer U, Wildermuth S, et al. Segmental arterial
and pancreaticoduodenal artery aneurysms: a complication of mediolysis: CTA findings at presentation and follow-up. AJR Am
pancreatitis causing spontaneous gastrointestinal hemorrhage. J Roentgenol 2006;187:1463.
Surgery 1980;88:335. 159. Shimohira M, Ogino H, Sasaki S, et al. Transcatheter arterial embo-
139. Guijt M, Delden OM, Koedam NA, et al. Rupture of true aneurysms lization for segmental arterial mediolysis. J Endovasc Ther 2008;
of the pancreaticoduodenal arcade: treatment with transcatheter 15:493.
arterial embolization. Cardiovasc Intervent Radiol 2003; 26:166.
C H A P T E R
12
Hepatic, Splenic, and Portal
Vascular Systems
Karim Valji
ANATOMY
ARTERIOGRAPHY AND VENOGRAPHY
Development
Techniques for celiac and superior mesenteric arteriog-
raphy are described in Chapter 11. Splenic or common The liver bud develops between the pericardial cavity and
hepatic arteriography is performed with a variety of the stalk of the primitive yolk sac.4 Liver cords insinuate
catheters, including cobra and sidewinder shapes. Steer- between tributaries of the vitelline and umbilical veins to
able, hydrophilic guidewires simplify catheter place- form the hepatic sinusoids. Branches of the right vitelline
ment. Alternatively, high-flow coaxial microcatheters veins around the duodenum develop into the central por-
are used to select the main splenic or hepatic arteries tal veins.5 The right umbilical vein involutes, and the left
and their branches. umbilical vein becomes the primary inflow vessel to the
The hepatic veins are studied from an internal jugu- liver. The hepatic venous outflow is directed toward the
lar (IJ) vein approach using a multipurpose angio- upper portion of the right vitelline vein, which ultimately
graphic or cobra-shaped catheter. In a small percentage forms the hepatic veins and the intrahepatic portion of the
of patients, a femoral route is necessary because of the IVC. The ductus venosus connects the left umbilical vein
downgoing orientation of the main hepatic vein enter- (portal venous inflow) to the right vitelline vein (hepatic
ing the inferior vena cava (IVC). This situation may outflow). Shortly after birth, the ductus venosus and left
occur after some liver transplantations or with hepatic umbilical vein close and form the ligamentum venosum
vein anomalies (see later discussion). Wedged hepatic and ligamentum teres, respectively.
vein manometry and venography are done with a bal-
loon occlusion catheter inflated within a peripheral Normal Anatomy
hepatic vein branch or a 5-French (Fr) endhole catheter
advanced into a peripheral vein until resistance is met. Liver
A flat pressure waveform indicates a wedged position. With the advent of living-related split-liver donor trans-
Measurements should be obtained before contrast in- plants, more ambitious surgical techniques for segmental
jection, which may spuriously elevate the sinusoidal hepatic resection, and transcatheter methods for treatment
pressure. Overinjection can produce subcapsular ex- of liver tumors, a detailed understanding of the normal,
travasation and liver perforation. Retrograde filling of variant, and collateral hepatic circulations is critical for the
the portal vein is enhanced when CO2 is used as the vascular interventionalist. For preoperative planning,
contrast agent (30 to 60 cc of gas injected rapidly). high-quality computed tomography (CT) or magnetic
The splenic, superior mesenteric, and portal veins are resonance (MR) arteriography and venography are both
visualized on the late phases of celiac or superior mes- extremely accurate.6-9 For transarterial therapy, selective
enteric arteriography (indirect portography). Direct digital angiography is required, including celiac and supe-
splenoportography is rarely required in the evaluation rior mesenteric arteriography, right and left hepatic arteri-
of patients with portal hypertension.1 Iodinated contrast ography, and often more subselective catheterization.10,11
or CO2 (15 to 20 cc) is injected through a micropuncture The liver is divided into right and left lobes separated
catheter inserted into the substance of the spleen with by the major fissure. The right lobe has anterior and poste-
ultrasound guidance. The tract is embolized with Gel- rior segments; the left lobe has medial and lateral seg-
foam as the catheter is withdrawn.2,3 ments. The caudate lobe is anatomically distinct from the
356
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 357
right and left lobes. By convention, segmental anatomy is becomes the proper hepatic artery. This vessel enters the
based on the original system of Couinaud demarcated by porta hepatis and divides into the right hepatic artery
the three main hepatic veins and a transverse plane at the (RHA) and left hepatic artery (LHA), which feed their
level of the portal vein bifurcation12,13 (Fig. 12-1). How- respective lobes. The RHA supplies segments V to VIII
ever, the relationship between these landmarks identified (and sometimes segment I, caudate lobe). The LHA sup-
on cross-sectional imaging and the true anatomic seg- plies segments II, III, IVa, and IVb. The inconsistent
mental anatomy is only approximate. middle hepatic artery, which, if present, supplies segments
The liver is supplied by the common hepatic artery IVa and IVb, usually originates from the right hepatic
and portal vein. Normally, about three fourths of the artery or forms a true trifurcation. Variations in hepatic
blood supply to the liver comes from the portal vein. arterial anatomy are common (see later discussion). Al-
Any reduction in hepatic arterial or portal venous blood though the hepatic arteries are considered end arteries,
flow leads to a compensatory increase in flow through intrahepatic and extrahepatic anastomoses do exist. The
the companion system. The biliary tree is nourished by origins of important branches are outlined in Table 12-1.
branches of the hepatic arteries. The portal vein (PV) is formed by the confluence of the
The common hepatic artery arises from the celiac artery superior mesenteric vein (SMV) and splenic vein14 (Fig. 12-3).
(Fig. 12-2). After giving off the gastroduodenal artery, it It is valveless. Normal main portal vein pressure is about
II
IVa
I
VIII
VII
III
IVb
VI Portal vein
VII
VI
B C
FIGURE 12-1 Segmental anatomy of the liver. A, Schematic drawing shows segmental divisions along with portal vein inflow and
hepatic vein outflow. Segment I (caudate lobe) lies posterior to segments III and IV and in front of the inferior vena cava. Computed
tomography scans through the upper (B) and lower (C) aspects of the liver, with segments noted. (A, Adapted with permission from the website
of the American Hepato-Pancreato-Biliary Association, www.ahpba.org.)
358 III. VISCERAL ARTERIES AND VEINS
A B
Left gastric
(coronary) vein
Portal
vein
Splenic vein
Gastrocolic
vein
Inferior
Superior mesenteric
mesenteric vein
vein
A B
FIGURE 12-3 Portal venous anatomy. A, Schematic drawing. B, Direct transhepatic portogram through an obstructed transjugular
intrahepatic portosystemic shunt. (A, From Lundell C, Kadir S. The portal venous system and hepatic vein. In: Kadir S, editor. Atlas of normal and
variant angiographic anatomy. Philadelphia: WB Saunders; 1991, p. 370.)
A B
FIGURE 12-4 Hepatic venous anatomy. A, Schematic drawing. B, Normal right hepatic venogram.
A B
FIGURE 12-6 A, Normal splenic arteriogram showing the dorsal pancreatic (D), transverse pancreatic (T), pancreatica magna (M), and
omental (O) branches. Proxaimal irregularity is guidewire-related spasm. B, Late-phase indirect splenoportogram. Diminished density in the
main portal vein (arrow) is caused by unopacified inflow from the superior mesenteric vein.
A B
C
362 III. VISCERAL ARTERIES AND VEINS
Classic PV anatomy is found in 65% to 75% of the With splenic artery obstruction, several collateral
population. Surgically significant variants involve routes are available:
trifurcation of the main PV (type 2, 9% to 16%), origin
Left gastric to short gastric arteries
of the right posterior branch from the main PV (type 3
Right gastroepiploic to left gastroepiploic artery
or Z type, 8% to 13%), and separate segment VI
(see Fig. 11-14)
or VII branches from the right portal vein (types 4 and
Pancreatic arcades or dorsal pancreatic artery to
5, 7%).17,26
distal pancreatic arteries
Accessory right hepatic veins are found in 25% or
more of the population (Fig. 12-8). In about 3% of indi- Patterns of collateral flow in the portal and hepatic
viduals, an inferior right hepatic vein (entering the IVC venous systems are discussed subsequently.
well below the diaphragm) is the dominant venous
drainage for the right lobe.16
MAJOR DISORDERS
Collateral Circulation
Cirrhosis and Portal Hypertension
With extrahepatic arterial obstruction, the major collateral (Online Case 68)
pathways into the liver are from:
Etiology
SMA to pancreaticoduodenal arcades and
Cirrhosis is a progressive liver disease characterized by
choledochal arteries (see Fig. 11-13)
generalized necrosis, regeneration, and widespread fibro-
Diaphragmatic inferior phrenic branches to
sis.27 Initially, inflammation or steatosis predominates.
intrahepatic arteries (Fig. 12-9)
Fibrotic tissue then infiltrates the sinusoidal spaces and
Splenic artery to pancreatic, gastric, and gastro-
obstructs central veins while preserving portal venules.
epiploic branches
Masses (either micronodular or macronodular) begin to
With intrahepatic arterial obstruction, the liver is pri- form, including regenerative, dysplastic, and malignant
marily supplied by accessory hepatic arteries (if present) lesions. As the vascular resistance in the liver increases,
and extracapsular branches. PV pressure rises, but flow is still directed into the liver
(hepatopetal). An imbalance in the relative activity of vaso-
dilators (e.g., nitric oxide) and vasoconstrictors (e.g., en-
dothelin-1) is responsible for the disturbances in hepatic,
splanchnic, and peripheral hemodynamics that follow.28,29
With progression of cirrhosis, systemic and splanchnic
vasodilation occurs, leading to increased cardiac output
(a hyperdynamic circulatory state) and humorally medi-
ated renal and hepatic vasoconstriction, which further
impedes liver blood flow.30,31 Extrahepatic portal flow in-
creases while intrahepatic portal flow decreases; in a
compensatory fashion, hepatic arterial flow is augmented.
With end-stage cirrhosis, the liver shrinks, and por-
tal venules and hepatic arterial branches are severely
compressed by fibrotic infiltration and regenerating
nodules. Hepatic vein outflow drops substantially. Intra-
hepatic pressure becomes so great that the portal system
is decompressed through portosystemic collateral chan-
nels (see later discussion). Ultimately, flow in the PV is
completely reversed (hepatofugal).
Although cirrhosis is by far the most frequent cause of
portal hypertension, many other diseases can produce
similar physiologic effects. Portal hypertension is tradition-
ally classified by the site of obstruction relative to the he-
patic sinusoids32 (Boxes 12-1 through 12-5). Some diseases
affect one level and then extend to others. Disorders that
FIGURE 12-8 Accessory inferior right hepatic vein (arrow) on cause elevated portal pressures proximal to or beyond the
coronal maximum intensity projection magnetic resonance venogram. hepatic sinusoids are considered later in this chapter.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 363
A B
FIGURE 12-9 Acute occlusion of liver transplant hepatic artery (HA). A and B, Celiac arteriography shows complete HA obstruction
along with collateral circulation from the right inferior phrenic artery (long arrow) and dorsal pancreatic artery (short arrow) into the intrahepatic
branches (open arrow).
F O R M S O F P O RTA L C AU S E S O F
H Y P E RT E N S I O N PRESINUSOIDAL
I N T R A H E PAT I C
Extrahepatic portal vein obstruction (see Box 12-2) OBSTRUCTION
Presinusoidal intrahepatic obstruction (see Box 12-3)
Sinusoidal intrahepatic obstruction (see Box 12-4) Hepatitis
Postsinusoidal obstruction (see Box 12-5) Biliary cirrhosis
Hyperdynamic portal hypertension Primary form
Chronic obstruction
Schistosomiasis
Toxic agents (e.g., vinyl chloride, cytotoxic drugs)
Metabolic disorders (e.g., hemochromatosis)
BOX 12-2 Malignancies
Myeloproliferative disorders
C AU S E S O F P O R T A L V E I N Reticuloendothelial tumors
OBSTRUCTION Sarcoidosis
Congenital hepatic fibrosis
Thrombosis (bland or neoplastic invasion) Idiopathic portal hypertension
Extrinsic compression
Tumor
Inflammatory mass
Postoperative
Congenital
364 III. VISCERAL ARTERIES AND VEINS
variceal size and stigmata of recent rupture (e.g., red occult hepatic malignancies. The primary indications for
wheals, cherry spots). Endoscopy may also identify an diagnostic invasive procedures are confirmation or
unrelated reason for acute gastrointestinal bleeding. quantitation of portal hypertension and transvenous
Ascites is another important complication of portal liver biopsy.
hypertension. The causes of ascites are manifold. Increased
splanchnic blood flow elevates microcirculatory pres- HEPATIC VEIN MANOMETRY
sures and increases production of lymph, which leaks Direct measurement of PV pressure is hardly ever needed
from the liver and intestines.41 In addition, peripheral for diagnosing portal hypertension; clinical studies have
arterial dilation (a response to vasoactive factors liber- shown that the hepatic vein wedged (HVW) pressure is
ated from the gastrointestinal tract) leads to a reduction equal to PV pressure in most patients.44 The difference
in effective plasma volume and retention of salt and between HVW and IVC (or right atrial) pressure is the
water by the kidneys. The hepatic lymphatic system corrected sinusoidal pressure, which reflects the portosys-
becomes overwhelmed, causing peritoneal leakage and a temic gradient. However, the measurements are valid only
vicious cycle of further reduction in the plasma volume when the PVs and hepatic sinusoids are in continuity. In
and worsening ascites. patients with extrahepatic PV obstruction, splenic vein
Cirrhotic patients also are at risk for hepatic encepha- obstruction (segmental portal hypertension), or presi-
lopathy, spontaneous bacterial peritonitis, splenomegaly nusoidal portal hypertension, this disconnection leads to
and pancytopenia, hepatocellular carcinoma, and ulti- a spuriously low HVW pressure. Normally, the portosys-
mately complete hepatic failure. Less frequent complica- temic gradient is less than 5 mm Hg. Portal hypertension
tions include hepatorenal syndrome, hepatopulmonary is defined as a gradient more than 6 mm Hg. The risk of
syndrome, portopulmonary hypertension, and hepatic bleeding from gastroesophageal varices becomes signifi-
hydrothorax. Some of these conditions are related to cant when the gradient is greater than 12 mm Hg.40
the misregulation of vasodilating and vasoconstricting
factors.42 Hepatorenal syndrome is characterized by dif- HEPATIC VENOGRAPHY
fuse splanchnic and peripheral vasodilation and de- Free hepatic venography is done to assess the hepatic
creased effective plasma volume, prompting reflex renal veins if obstruction is suspected, during the trans-
vasoconstriction.43 Whereas the chronic form is treat- jugular intrahepatic portosystemic shunt (TIPS)
able, the acute type is almost universally fatal (see later procedure, and sometimes during transvenous liver
discussion). biopsy. Balloon-occluded or catheter-wedged hepatic
venography with CO 2 is routinely performed be-
Imaging and Tissue Diagnosis fore creating TIPS to provide a target for the PV
Virtually all patients with suspected cirrhosis or portal puncture. Hepatic veins have a pinnate (feather-like)
hypertension undergo radiologic tests to prove the exis- branching pattern; portal veins branch dichotomously
tence and assess the extent of liver disease and to detect (Fig. 12-10).
A B
FIGURE 12-10 A, Wedged hepatic venography shows homogeneous parenchymal stain and filling of adjacent hepatic venules and veins.
B, Carbon dioxide wedged hepatic venography using an occlusion balloon (arrow) with backfilling of gas that outlines the portal vein.
366 III. VISCERAL ARTERIES AND VEINS
ARTERIOGRAPHY AND INDIRECT PORTOGRAPHY collateral pathways, which include the following prin-
With advanced cirrhosis, the hepatic arteries take on a cipal channels (Fig. 12-13):
corkscrew appearance because of increased arterial
flow and liver shrinkage, and the spleen and splenic Left gastric (coronary) and short gastric veins
artery are enlarged (Fig. 12-11). The demand for hepatic through gastroesophageal veins to the azygous
artery flow can become so great that flow in the gastro- venous system
duodenal artery is reversed. Occasionally, arterioportal Left PV through a paraumbilical vein to
shunting is seen (Fig. 12-12). systemic abdominal wall veins around the
In the early stages of cirrhosis, PV flow is relatively umbilicus (caput medusae) or internal iliac
normal. As the disease advances and portal hyperten- veins
sion becomes significant, several changes occur. The Splenic or short gastric veins through retroperito-
most important is the appearance of portosystemic neal branches to the left adrenal/inferior phrenic
A B
FIGURE 12-12 Advanced cirrhosis with global shunting from hepatic artery (A) to portal vein (B) seen on celiac arteriography.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 367
A B
C D
FIGURE 12-13 Portosystemic collateral pathways. A through C, On reformatted coronal computed tomography (CT) scans, blood is diverted
up the coronary vein (arrowhead), through large gastroesophageal varices (black arrows), and then to the azygous venous system (white arrow).
Note shrunken nodular liver, enlarged spleen, ascites, and large bilateral pleural effusions. Paraumbilical vein drains the left portal vein
through internal iliac venous channels into the inferior vena cava seen on CT scan (D, arrow).
Continued
368 III. VISCERAL ARTERIES AND VEINS
E F
G H
FIGURE 12-13, contd E, Early and (F) late phases of a direct portogram. Splenorenal shunt drains short gastric varices from the splenic
hilum into the left renal vein (arrow), and then the inferior vena cava on early (G) and late (H) phases of a direct splenic venogram through a
transjugular intrahepatic portosystemic shunt.
I J
K
FIGURE 12-13, contd Such shunts are occasionally embolized to prevent bleeding, relieve hepatic encephalopathy, or improve overall liver
perfusion (I). Cecal varices (arrow) fill by direct portal vein injection (J) and then drain through systemic pelvic collaterals into the inferior vena
cava (K, arrow).
vessel (Fig. 12-16). A stainless steel stiffening cannula RESULTS AND COMPLICATIONS Liver tissue can
is placed through the sheath. A flexible biopsy needle be extracted in more than 97% of attempts. It may
(e.g., Quick-Core or TLAB Patel set) is then inserted be slightly more difficult to obtain tissue in liver trans-
through the cannula and torqued within the hepatic plant patients with a piggyback type hepatic vein
vein until resistance is met. The device is buried anastomosis47 (see later discussion). Biopsy samples are
in the parenchyma and triggered, and a piece of adequate for pathologic diagnosis 96% to 97% of the
tissue is removed. Three or four specimens are time.48-52 The major risk of the procedure is liver capsule
needed to ensure that sufficient material is obtained perforation. Minor complications (including access site
for diagnosis.45,46 bleeding and cardiac dysrhythmias) are reported in up
370 III. VISCERAL ARTERIES AND VEINS
A B
C D
FIGURE 12-14 Duodenal varices treated with embolotherapy. A, Late phase of celiac arteriogram shows splenic hilar varices and duodenal
varices (arrow). B, The duodenal varices are better seen with selective gastroduodenal arteriography through a coaxial microcatheter. C, Pelvic
collaterals were found to drain into the right ovarian vein and then into the inferior vena cava. D, The ovarian vein is catheterized, a micro-
catheter is negotiated to the site of the varices, and ethanolamine oleate was injected to induce sclerosis.
BALLOON-OCCLUDED RETROGRADE
TRANSVENOUS OBLITERATION OF GASTRIC
AND DUODENAL VARICES
In Japan and other parts of Asia, balloon-occluded retro-
grade transvenous obliteration (BRTO) has become a
popular modality for prevention or control of bleeding
from isolated variceal clusters.63-65 Gastric and duodenal
varices are notoriously difficult to treat with endoscopy
because of their location and size. In some individuals,
these massive shunts can also cause intractable hepatic
encephalopathy.
FIGURE 12-15 Hepatofugal flow in the portal vein on direct Before BRTO, indirect portography via celiac and
injection through a TIPS.
SMA arteriography is done to establish the portal ve-
nous anatomy and hemodynamics. The outflow vein
to these measures. Intractable ascites can have a marked for the varices (typically the left inferior phrenic/
impact on overall quality of life. In such cases, frequent adrenal to left renal vein for gastric varices, right go-
large volume paracentesis (#4 to 5 L) is necessary to di- nadal vein for duodenal varices) is selectively engaged
minish pain, nausea, and respiratory compromise. The with a diagnostic catheter (see Fig. 12-14). A 6-Fr bal-
application of volume expanders (e.g., intravenous [IV] loon occlusion catheter (e.g., 11- or 20-mm diameter) is
albumin infusion) in this setting is controversial. How- advanced into the main trunk and inflated, and ve-
ever, large volume paracentesis is inconvenient for pa- nography is performed to classify the varices and col-
tients and does have risk. lateral veins.
A B
FIGURE 12-16 Transjugular liver biopsy in a posttranplant patient. Note prior coil embolization of gastroesophageal varices and
placement of stents for portal vein stenosis. A, An angled catheter and sheath have been advanced well into the middle hepatic vein and
venography done. B, With the metal cannula in place within the sheath, the entire mechanism is rotated anteriorly. The inner biopsy needle is
advanced into the liver parenchyma and triggered to obtain liver tissue.
372 III. VISCERAL ARTERIES AND VEINS
A B
C
FIGURE 12-17 Transjugular intrahepatic portosystemic shunt (TIPS) procedure with hepatocellular carcinoma and portal vein (PV) throm-
bosis. A, Contrast-enhanced magnetic resonance image shows a large hypervascular heterogeneous mass invading most of the right lobe of the
liver. Right and left main portal veins are patent. Patient suffered several variceal bleeds, and a shunt was requested as a palliative measure.
B, By the time the TIPS was performed, the tumor had invaded the portal vein (long arrow), and cavernous transformation has begun to
bypass the obstructed PV (arrowheads). Note retrograde flow into the splenic vein (short arrow) and inferior mesenteric vein (curved black arrow).
C, A portosystemic shunt was created with two Viatorr stent grafts from the patent central portal vein to the inferior vena cava.
A B
C D
FIGURE 12-18 Transjugular intrahepatic portosystemic shunt procedure with portal vein thrombosis. A, Entry is made into a distorted
portal venous system. A stiff angled glidewire was ultimately advanced into the main portal vein. B, Portography shows tapered occlusion of
the main portal vein (long arrow). Prominent gastric varices are seen (short arrow) along with a splenorenal shunt (C, arrowheads). D, Viatorr
stent graft has been inserted; shunt is widely patent.
angiography is certainly better for assessing these param- However, deep sedation or general anesthesia admin-
eters (PV patency, status of the hepatic veins, degree of istered by a dedicated anesthesiologist is mandatory
ascites, liver size, presence of liver tumors or polycystic in unstable or uncooperative patients and helpful in
liver disease). Just as important, the operator can deter- all cases.
mine beforehand the suitability of the individual hepatic The standard access site is the right IJ vein (Fig. 12-19).
veins along with the best trajectory and distance to the The left IJ vein is preferred by some operators and should
portal vein. be considered if a second try is made after a failed first
The TIPS procedure can be performed with moderate attempt. A 40-cm 10-Fr vascular sheath is advanced
sedation under the direction of the interventionalist. into the right atrium. Right atrial and IVC pressures are
376 III. VISCERAL ARTERIES AND VEINS
A B
measured. If right atrial pressure is markedly elevated Several methods are used to guide the puncture from
(#20 to 25 mm Hg), the interventionalist should proceed the hepatic vein toward the PV (Fig. 12-21). The most
with caution. Fulminant right heart failure can occur popular techniques are as follows:
after the shunt is created. 1. Reliance on bony landmarks. The right PV trunk
The right or middle hepatic vein is entered with a typically runs at the level of the 11th rib, about 0.5
multipurpose angiographic catheter and steerable to 1.5 vertebral widths from the lateral border of
guidewire. If the right hepatic vein is small, has a very the spine.97
acute angle with the IVC, or is difficult to catheterize, 2. Injection of CO2 through a balloon occlusion
TIPS can be created from the middle (or even left) catheter to fill the central portal venous
hepatic vein. It is important to establish which vein is system98 (see Fig. 12-19).
being used so that the intrahepatic puncture toward the 3. Using CT guidance to place a metallic coil
PV is made in the appropriate direction. This step can be adjacent to the intended entry site on the
accomplished with steep oblique/lateral fluoroscopy or portal vein as a fiduciary marker.
ultrasound interrogation. About 3% of the population 4. Ultrasound-guided catheterization of an enlarged
has a dominant inferior right hepatic vein. In this situ- paraumbilical vein. A catheter advanced into the
ation, TIPS must be formed from the right common central portal venous system serves as a target
femoral vein (Fig. 12-20; see also Fig. 12-8). for needle passes.99
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 377
D E F
FIGURE 20-19, contd A marking pigtail was advanced for direct portography (D). The distance from portal vein entry to inferior vena cava
entry was measured at 6 cm (arrowheads). E, A 10 mm & 2 cm & 6 cm Viatorr stent graft was inserted. Repeat portography shows a widely patent
shunt with no filling of intrahepatic portal venous branches. Portosystemic gradient was 6 mm Hg. F, The coronary vein was catheterized.
Gastroesophageal varices still opacify with forced injection, but portal decompression has been achieved and embolization is not necessary.
A B C
FIGURE 12-20 Femoral transjugular intrahepatic portosystemic shunt (TIPS) procedure. A, From right internal jugular vein access,
the major draining vein is an inferior right hepatic vein. TIPS cannot be created from above. B, Through a right common femoral vein
approach, the standard TIPS set is used to enter the right portal vein. C, An uncovered Wallstent is placed to create the shunt (procedure
done before advent of covered stents).
The site of PV puncture is critical. Because the portal set). The catheter-trocar is guided down the protective
vein bifurcation is extrahepatic in about one half of indi- outer sheath until they are tip to tip. When the right
viduals, entry should be at or peripheral to this point hepatic vein is used, the needle is turned anteromedially
to avoid extrahepatic puncture and the possibility of toward the right PV, and a brisk needle pass is made. From
exsanguinating hemorrhage.16,100 the middle hepatic vein, either an anterior or posterior
After the outer sheath is advanced well into the hepatic throw (toward the left or right portal vein, respectively)
vein, the stiffening cannula and catheter-needle system may be appropriate. After the sharp stylet is removed, the
are inserted (e.g., 16-gauge Roesch-Uchida catheter-trocar catheter is slowly withdrawn, and contrast is injected after
378 III. VISCERAL ARTERIES AND VEINS
BOX 12-8
TECHNICAL PEARLS
F O R D I F F I C U LT
TRANSJUGULAR
I N T R A H E PAT I C
P O RT O S Y S T E M I C S H U N T
A B
A B
FIGURE 12-23 Viatorr nitinol-ePTFE covered stent graft. A, Photograph of fully constrained device (top), partially uncovered device
(middle), and fully deployed device (bottom). B, Operative end of insertion catheter, with hemostatic valve at end and knob for pulling the rip
cord to release covered portion of device as a sidearm. (Courtesy of W.L. Gore and Associates.)
At the end of the procedure, a portal venogram is of varices should be considered (Fig. 12-24). On occa-
done to document shunt patency, lack of filling of intra- sion, thrombi will form within the shunt while the
hepatic PV branches, and nonvisualization of gastro- procedure is ongoing. The reason is often obscure, but
esophageal varices. If the portosystemic gradient incomplete track coverage, portal vein dissection, or
remains elevated despite use of a 12-mm balloon, vari- unsuspected thrombophilia are possible. If the patient
ces continue to fill with portal injection, or the patient has not recently bled, full anticoagulation and treatment
recently had massive variceal bleeding, embolization with fibrinolytic agents may be helpful. If bleeding is
380 III. VISCERAL ARTERIES AND VEINS
A B
C D
FIGURE 12-24 Variceal embolization after a transjugular intrahepatic portosystemic shunt (TIPS) procedure. A, Post-TIPS portography
shows a widely patent shunt, which extends up too far into the right atrium (arrow). No varices fill, but patient has suffered very recent
massive variceal hemorrhage. B, Coronary vein catheterization with an angled catheter outlines the varices. C, Through a guiding sheath,
an Amplatzer plug is being advanced. D, The occluder has been deployed (arrow), completely obstructing the coronary vein.
a concern, maceration or mobilization of clot with hemorrhage, early rebleeding (before 6 months) oc-
a dilation or occlusion balloon is appropriate. Over- curs less than 15% of the time. TIPS is more effective
night anticoagulation is advisable when these steps are than sclerotherapy or banding in preventing rebleed-
necessary. ing, although survival may not be prolonged in all
Postprocedure care includes observation for signs of populations.71,76 About 50% to 75% of individuals
abdominal bleeding, evaluation of hepatic and renal treated for refractory ascites have partial or complete
function, treatment of encephalopathy, and follow-up resolution within about 1 month of placement.77,78,104
duplex sonography of the shunt. Because of air trapped Early (30-day) mortality after TIPS can be substantial
in the graft fabric, Viatorr stent visualization by ultra- (3% to 45%), but this is largely because of underlying
sound is only possible days after deployment. liver disease rather than direct complications of the
procedure.105
Early Results The direct intrahepatic portosystemic shunt (DIPS) is an
A shunt can be created successfully in more than 90% endovascular alternative to TIPS. The portosystemic
to 95% of attempts, leaving a portosystemic gradient communication is made between the IVC and the portal
less than 12 mm Hg or reduced by greater than 50% in vein using intravascular ultrasound (IVUS) guidance.106
most cases.31,71,73,102,103 In patients treated for variceal Reported results are promising.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 381
Complications persistent hyperbilirubinemia may be related to hemo-
Major procedure-related complications develop in about lysis. Fulminant hepatic failure is rare unless the patient
3% to 5% of patients. Table 12-4 lists adverse events.* already had end-stage liver disease.
Other problems include acute renal failure, access site The immediate mortality rate is up to 2%, although
bleeding, cardiac dysrhythmias, and reactions to con- this figure may be higher for less experienced opera-
trast material. tors. Early procedure-related death is usually the
The riskiest step in the TIPS procedure is the trans- result of massive bleeding from extracapsular or cen-
hepatic needle puncture. Liver capsule perforation and tral vessel perforation, hepatic artery thrombosis with
injury to small hepatic artery or bile duct branches are fulminant hepatic failure, or acute right heart failure.
common and usually inconsequential. Rarely, needle
passes cause gallbladder perforation, hepatic artery Late Results
pseudoaneurysms, or arteriovenous fistula formation. In the past, after a TIPS was created with a bare stent
Fatal hemorrhage from extracapsular, caval, right atrial, (e.g., Wallstent), a layer of pseudointima would slowly
or portal venous perforation is rare. Acute shunt throm- cover the track, which protected it from late throm-
bosis is reported in about 3% to 4% of cases and has bosis.111 Cellular and fibrous proliferative tissue lined
several causes108,109 (Box 12-9 and Fig. 12-25). the walls of the conduit and outflow veins. An inflam-
Hepatic encephalopathy is a major concern after any side- matory reaction to injured bile ducts was an impor-
to-side portosystemic shunt. With diversion of mesenteric tant cause of this process.112 Significant stenoses
venous blood, nitrogen-containing compounds (among developed within the body of the stent and the out-
several other substances) produced by bacterial action in flow vein; however, PV stenoses were exceedingly
the gut are not metabolized by the liver before entering uncommon.
the circulation. Blood ammonia levels can rise sharply Despite excellent short-term results using the un-
and result in encephalopathy. In this population, enceph- covered Wallstent, most of these shunts did not remain
alopathy also may be related to increased protein intake, patent without repeated intervention. The reported pri-
gastrointestinal bleeding, sepsis, dehydration, or acute mary patency rate for TIPS with these devices is 25%
hepatitis. This complication is more likely when the re- to 66% (average, 50%) at 1 year and 26% to 32% at
sidual portosystemic gradient is less than 10 mm Hg.110 2 years.113-115
Although about 25% to 30% of patients develop new or There is incontrovertible evidence that PTFE-covered
worsened encephalopathy, less than 5% to 10% are unre- stent-grafts dramatically improve long-term durability,
sponsive to medical therapy; those individuals may be with 1-year primary patency rates of about 81% to 86%,
candidates for shunt reduction (see later discussion). and 2-year rates of about 80%.103,107,116 Survival at 5 years
A transient (and sometimes profound) elevation in after TIPS is about 61% with a 10% rebleeding rate; these
liver enzymes is common after TIPS. However, isolated outcomes are comparable to those achieved with surgi-
cal shunts and are certainly better than best medical
*See references 73, 102, 103, 105, 107. therapy and endoscopy.71,76,117
Transcapsular puncture 33
C AU S E S O F A C U T E
Bleeding TRANSJUGULAR
Intraperitoneal 1-13 I N T R A H E PAT I C
Hemobilia 1-4 P O RT O S Y S T E M I C S H U N T
Liver dysfunction THROMBOSIS
Transient worsening 10-20
Fulminant hepatic failure or 3-7
infarction Thrombophilia (see Boxes 1-4 and 1-5)
Hepatic encephalopathy Uncovered portion of shunt track
New onset or worsened 10-44 Portal vein dissection
Uncontrollable 5-10 Low flow (e.g., competing flow through
Sepsis 2-10
splenorenal shunt)
Stent malposition or migration 1-3
Other Preexisting portal or mesenteric vein thrombus
Fistula %1 Residual shunt stenosis
Infection of TIPS %1
382 III. VISCERAL ARTERIES AND VEINS
A B
Surveillance and Shunt Management sonography is the best tool for long-term screening
Recurrent variceal hemorrhage or return of intractable because of its simplicity and low cost. Sonography
ascites after TIPS procedure is usually a sign of shunt was routinely performed immediately following and
stenosis or occlusion (see Box 12-9). Because shunt 1 month after the TIPS procedure, at 3-month intervals
obstruction may be silent, vigorous imaging surveil- for the first year and at 6- to 12-month intervals there-
lance programs are routine. CT angiography is helpful after. However, the necessity of this approach has been
in detecting impending TIPS failure, but color Doppler questioned following widespread adoption of covered
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 383
stents. In the era of stent grafts, the timing of imaging TIPS is placed. In these cases, portal venous flow can be
protocols is hotly debated.118 augmented in several ways125-128 (Fig. 12-27):
Several findings may signal shunt dysfunction119-123
Shunt occlusion is accomplished by embolization
(Box 12-10). However, it has recently become apparent
with coils or an Amplatzer plug. Obviously, the
that color Doppler sonography is not as accurate in
patient will then be at risk for the symptoms
detecting shunt dysfunction as was once thought.
of portal hypertension for which he or she was
Although quite specific in identifying abnormalities
first treated. More importantly, cases of life-
(about 90%), sonography is not particularly sensitive in
threatening or fatal cardiovascular collapse
this regard (about 50%).73 Therefore shunt angiography
because of abrupt hemodynamic changes have
is advisable if varices reappear at endoscopy or the
been reported.129
clinical scenario suggests shunt malfunction.
Shunt reduction is achieved in several ways, most
A direct portal venogram is performed from a right
of which involve placement of a covered, partially
IJ vein approach. A patent shunt almost always can be
constrained stent within the existing shunt. Some
cannulated with an angiographic catheter (e.g., multi-
of these devices, fashioned sterilely on the
purpose angiographic or cobra shape) and an angled
interventional table, can later be adjusted using
hydrophilic guidewire. Care must taken to avoid
balloons to achieve controlled reduction in shunt
unknowingly passing through the interstices (rather
flow.
than the mouth) of the uncovered portion of the stent.
Splenorenal shunt embolization using the BRTO
The presence of shunt occlusion, stenosis of greater
method (see earlier discussion) can be effective
than 50%, portosystemic gradient of greater than 12 mm
in appropriate patients with intractable encepha-
Hg, or filling of gastroesophageal varices are indica-
lopathy.
tions for intervention. If a bare stent was placed origi-
nally, insertion of a Viatorr device that extends from the
portal vein up to the IVC is appropriate (Fig. 12-26). Portal and Splenic Vein Thrombosis
With covered stents, in-stent stenosis is much less
common. In most cases, lesions develop in unstented Etiology
portions of the outflow hepatic veins, which then Portal vein thrombosis has many causes130,131 (Box 12-11).
require placement of additional covered stents. Stents It was once thought that most cases were idiopathic.
should not extend deep into the IVC, because caval In fact, a precipitating condition can be identified
thrombosis can result.124 in up to 80% of affected individuals. The etiology is
Occasionally, patients suffer uncontrollable hepatic often multifactorial. In children, sepsis is frequently
encephalopathy or progressive liver failure after the responsible.
PV thrombosis can be confined to the PV itself or
include the SMV but spare mesenteric vessels, or it can
entail widespread involvement (with or without an
BOX 12-10 adequate collateral circulation).
Splenic vein thrombosis is usually a consequence of
SONOGRAPHIC SIGNS pancreatitis, pancreatic neoplasms, splenectomy, throm-
OF TRANSJUGULAR bophilic states, or trauma.132,133 With obstruction of the
I N T R A H E PAT I C splenic vein, segmental or left-sided portal hyperten-
P O RT O S Y S T E M I C S H U N T sion may develop. The spleen then drains through several
DYSFUNCTION portoportal collateral routes (see later discussion).
A B
A B
FIGURE 12-27 Shunt reduction in a patient with liver failure following transjugular intrahepatic portosystemic shunt procedure.
Initial portogram showed a widely patent shunt. A suture was used to make a waist around the middle of a covered Viatorr stent, which was
then inserted into the existing shunt (A). B, Follow-up portogram demonstrates flow both in the shunt and the intrahepatic portal vein.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 385
Imaging
CROSS-SECTIONAL TECHNIQUES
Portal and splenic vein thrombosis are detected with
color Doppler sonography, or CT or MR angiogra-
phy.134,135 In the acute phase of the illness, signs of the
underlying causes (e.g., neoplasm, cirrhosis, pancreati-
tis, recent splenectomy) may be evident along with
thrombus in the portal, splenic, superior mesenteric,
and/or branch mesenteric veins. Ancillary findings are
bowel wall edema, varices, and ascites.
In the chronic phase, numerous collateral vascular
channels in the porta hepatis and gallbladder fossa
will bypass the obstruction and fill intrahepatic PVs.
Cavernous transformation is a misnomer for this
conditionthe PV itself remains occluded. Other porto-
portal and portosystemic collaterals may circumvent the
occlusion. Long after the acute event, calcification of the
PV, liver atrophy, and splenomegaly are possible.
CATHETER ANGIOGRAPHY
FIGURE 12-28 Cavernous transformation of the portal vein with
Because the obstruction in portal and splenic vein numerous collateral channels in the gallbladder fossa (arrow) is seen
thrombosis is proximal to the hepatic sinusoids, the on direct portography during transjugular intrahepatic portosystemic
normal pressures obtained at HVW manometry do not shunt procedure.
386 III. VISCERAL ARTERIES AND VEINS
A B
A B
FIGURE 12-30 Budd-Chiari syndrome. A, Contrast computed tomography scan shows a mottled parenchymal pattern and lack of filling
of central hepatic veins. Ascites is present. B, Color Doppler ultrasound fails to identify flow in the middle hepatic vein.
388 III. VISCERAL ARTERIES AND VEINS
A B
C D
FIGURE 12-31 Budd-Chiari syndrome from central hepatic vein thrombosis. A, The classic spider-web pattern with injection of the right
hepatic vein is caused by innumerable intrahepatic venous collaterals. B, Inferior venacavogram shows severe compression of its intrahepatic
segment because of a markedly enlarged caudate lobe. C, During TIPS procedure, carbon dioxide wedged hepatic injection outlines the portal
vein, providing a target for puncture. D, The portal vein has been entered. A Viatorr stent graft was subsequently placed.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 389
The TIPS procedure is valuable in many patients with Hepatic and Splenic Trauma
Budd-Chiari syndrome, sometimes as a bridge to trans- (Online Case 108)
plantation148,161-163 (see Fig. 12-31). A shunt improves
venous drainage from the liver. Etiology and Clinical Features
The liver and spleen are particularly susceptible to injury
SURGICAL THERAPY from blunt or penetrating abdominal trauma. Open or
Operative treatment options include mesenteric- laparoscopic surgical procedures are responsible for a
systemic shunts (e.g., mesoatrial shunt) and liver trans- significant number of cases. Arterial laceration can result
plantation. in parenchymal or peritoneal bleeding, subcapsular he-
matoma, pseudoaneurysms, or arteriovenous fistulas.168,169
Malignant Liver Neoplasms Although most patients with significant vascular injuries
(Online Cases 58, 79, and 89) are symptomatic, some show little evidence of massive
bleeding.
The liver is affected by a wide variety of benign and
malignant tumors (Box 12-12). Benign liver tumors are
Imaging
considered below. The role of the interventionalist in the
management of malignant lesions in adults164-167 is CROSS-SECTIONAL IMAGING
discussed in Chapter 24. In most centers, focused abdominal sonography in
trauma (FAST) has replaced diagnostic peritoneal lavage
as the screening tool for detecting posttraumatic intraab-
dominal hemorrhage.170 CT is the primary imaging
study for stable patients with blunt trauma. CT can ac-
curately stage the extent of injury to the liver or spleen
BOX 12-12 (Tables 12-5 and 12-6) and detect other abdominal or
LIVER NEOPLASMS pelvic injuries.171-174 Management decisions (observa-
tion, angiography, operation) are based on the clinical
Benign
picture and CT grade (Fig. 12-32).
Hemangioma CATHETER ANGIOGRAPHY
Adenoma
Focal nodular hyperplasia
With blunt trauma, arteriography shows extravasation,
Regenerating nodule
subcapsular or parenchymal hematomas, arterial occlu-
Biliary cystadenoma
sion, or diffuse punctuate injury (Fig. 12-33 and see
Malignant
Fig. 12-32). With penetrating trauma, typical findings
Hepatocellular carcinoma
include extravasation, pseudoaneurysms, and arterio-
Cholangiocarcinoma
venous fistulas (Fig. 12-34).
Angiosarcoma
Biliary carcinoma
Lymphoma
TABLE 12-5 AAST Computed Tomography Classification
Metastatic for Liver Trauma
Gastrointestinal tract
Breast Grade Injury Type
Pancreas I Subcapsular hematoma, %10% surface area
Lung Capsular tear, %1 cm deep
Kidney II Subcapsular hematoma, 10% to 50% surface area,
Islet cell (i.e., pancreas) %10 cm diameter
Capsular tear, 1-3 cm deep, %10 cm length
Carcinoid
III Subcapsular hematoma, #50% surface area
Pediatric Intraparenchymal hematoma, #10 cm or expanding
Metastases (e.g., neuroblastoma, Wilms Laceration #3 cm deep
tumor) IV Parenchymal laceration 25% to 75% of lobe or 1-3
Hepatoblastoma Couinaud segments
V Parenchymal laceration #75% of lobe or #4
Hemangioendothelioma
Couinaud segments
Hemangioma Juxtahepatic vein injury
Hepatocellular carcinoma VI Avulsion of liver
A B
D E
FIGURE 12-32 Blunt liver trauma from a motor vehicle crash. A and B, Contrast-enhanced computed tomography images show grade IV
liver injury with active bleeding and probable pseudoaneurysm (arrow). Also note perihepatic blood and left upper quadrant bleeding. C and
D, Common and selective right hepatic (RHA) arteriography show massive bleeding from the proximal RHA. E, The entire vessel was
embolized, and bleeding has ceased. No extravasation is noted from branches of the middle (long arrow) or left (short arrow) hepatic arteries.
392 III. VISCERAL ARTERIES AND VEINS
A B
FIGURE 12-33 Splenic artery embolization for abdominal trauma following a motor vehicle collision. A, Splenic arteriogram reveals
diffuse injury with irregular branch vessels and areas of gross and punctate extravasation. B, Following shower embolization with Gelfoam
pieces, the artery is occluded and bleeding is no longer seen.
C B
FIGURE 12-34 Bleeding hepatic artery pseudoaneurysm from percutaneous biliary drainage. Patient developed exuberant hemobilia
through the drainage catheter about one week after insertion. A, Hepatic arteriogram (done via SMA for replaced common hepatic artery)
shows no evidence of bleeding or culprit lesion. B, Tube was removed over a guidewire. Repeat angiography now reveals a pseudoaneurysm
(arrows). C, The involved branch was embolized distal and proximal to the lesion. Posttreatment angiography shows exclusion of the
aneurysm.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 393
to liver size, underlying liver disease, and vascular/ removal of the left lateral liver (segments II and III),
biliary anatomic variants.187,188 Rarely, catheter angiog- right trisegmentectomy (segments IV to VIII), left lobe
raphy is required before reduced-size transplants to (segments II, III, IVa, and IVb), or right lobe (segments
identify arterial variants, segmental blood supply, and V to VIII).190 The interventionalist must understand
the size of the donor artery. the precise operative anatomy in a particular case
before proceeding with diagnostic or interventional
Operative Procedures procedures.
In the classic orthotopic liver transplant procedure,
the hepatic arterial anastomosis is made between the Complications
donor celiac axis or common hepatic artery and the Up to 15% of patients suffer vascular complications after
recipient common hepatic artery. When the recipient liver transplantation. Because often they are initially
has two arteries supplying the liver (e.g., replaced silent and the clinical course may be hard to differentiate
right hepatic artery), a common trunk is created. Occa- from graft rejection or primary nonfunction, routine
sionally, an infrarenal iliac artery homograft is used imaging of transplants with noninvasive imaging (ultra-
(Fig. 12-35). The PV anastomosis is created in an end- sound, CT, or MR) is crucial.191-194
to-end fashion. An iliac vein interposition graft to the
SMV may be required if the recipient PV is diseased. HEPATIC ARTERY THROMBOSIS
The IVC connection can be fashioned with both supra- The most frequent vascular complication after liver
hepatic and infrahepatic anastomoses. However, transplant is hepatic artery thrombosis, which occurs
many transplant surgeons now use the piggyback in 3% to 5% of cases, and more frequently in chil-
technique in which an end-to-side anastomosis is dren.192,195-198 The common causes are operative errors,
formed using the suprahepatic donor segment and progressive hepatic artery stenosis, rejection, and ar-
the hepatic vein confluence of the recipient. terial kinking. With the exception of some children, no
Segmental (reduced or split) liver transplantation extrahepatic arterial collaterals initially support the
allows for pediatric or adult transplants from either graft. Coupled with some loss of the normal recipro-
cadaveric or living donors and increases the overall cal relationship between portal and arterial liver flow,
number of available grafts.189 Surgical options include the graft will be in jeopardy. Since the biliary tree is
A B
FIGURE 12-35 Orthotopic liver transplant with the donor hepatic artery (A) fed by an iliac artery homograft anastomosed to the
recipients distal abdominal aorta (B).
394 III. VISCERAL ARTERIES AND VEINS
A B
D
FIGURE 12-36 Liver transplant hepatic artery thrombosis. A, Color Doppler ultrasound shows diminished hepatic artery peak velocity,
low resistive index, and parvus et tardus waveform. B, Catheter angiography confirms complete hepatic artery occlusion with minimal
collateral flow into the liver. The occlusion could not be crossed with a guidewire, but thrombolysis was done through a proximal
microcatheter. After about 12 mg of tissue plasminogen activator was infused, flow is restored in the hepatic artery (C). D, Ultrasound the
following day shows more normal appearance of waveform and improved resistive index.
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 395
exclusively supplied by the hepatic artery, bile duct INFERIOR VENA CAVA/HEPATIC VEIN OBSTRUCTION
ischemia occurs frequently without treatment, result- IVC and hepatic venous obstructions are virtually un-
ing in strictures, bilomas, or mucosal sloughing (isch- heard of after traditional orthotopic liver transplantation,
emic cholangiopathy). in that no hepatic vein anastomosis is created. However,
Hepatic artery thrombosis usually happens within stenoses are a serious problem in 1% to 17% of split liver
2 to 3 months of transplantation. Patients often show or piggyback transplants.209,213-216 Early postoperative
signs of fulminant liver failure, biliary leak, or sepsis. lesions are usually technical problems such as a tight
The diagnosis is made with Doppler ultrasound or suture line or venous kinking; late stenoses are a conse-
contrast-enhanced CT imaging. Catheterization is some- quence of fibrosis or neointimal hyperplasia around the
times required for confirmation. Endovascular throm- anastomosis. Suggestive symptoms and signs are wors-
bolysis, angioplasty, and stent placement may allow ening ascites, abdominal pain, leg edema, and signs of
graft salvage, but many patients require immediate graft dysfunction.
revascularization to avoid the need for retransplan- These obstructions are readily detected on Doppler
tation195,199,201 (Fig. 12-36). sonography or CT angiography. Direct catheter-based
pressure gradients are needed to confirm cross-sectional
HEPATIC ARTERY STENOSIS imaging findings (gradient #5 to 6 mm Hg). Because
Hepatic artery stenosis is less common than frank occlu- reoperation in this situation is technically difficult, most
sion.192,196,198 Most obstructions occur at the anastomosis surgeons favor endovascular treatment. Stent placement
and are because of technical errors, intimal hyperplasia, usually is necessary for durable results in adults217-220
or graft rejection. Even when stenoses do not threaten (Fig. 12-39). Operators should be aware that stent place-
graft viability, biliary duct ischemia complicated by ment in this location is treacherous (see Chapter 16 and
stricture formation is common (see earlier discussion). Fig. 16-31).
Sonographic signs of hepatic artery stenosis include a
parvus et tardus waveform, focal peak hepatic artery HEPATIC ARTERY PSEUDOANEURYSMS
velocity of greater than 200 to 300 cm/sec, a resistive These lesions may present some time after transplanta-
index less than 0.5, and a systolic acceleration time tion with fever, hemobilia, unexplained bleeding, graft
greater than 0.08 second in the intrahepatic arteries202-204 dysfunction, or arterial occlusion.185 Extrahepatic arterial
(Fig. 12-37). pseudoaneurysms are rare and potentially catastrophic.
Angioplasty of hepatic artery stenoses is techni- They develop at the hepatic arterial anastomosis and
cally successful in about 80% of cases.205,206 However, may have an infectious origin (Fig. 12-40). Intrahepatic
stenoses in fresh grafts ('2 weeks old) may rupture if pseudoaneurysms and arteriovenous fistulas usually are
opened with a balloon. Reported rates of restenosis caused by a postoperative percutaneous procedure.221,222
have been highly variable; stents may improve on these
results207,208 (see Fig. 12-37). Transplant hepatic arteries
are very prone to vasospasm and thrombosis. Only OTHER DISORDERS
floppy microwires (e.g., Synchro wire) should be used.
If occlusion occurs, liberal use of intraarterial nitro-
Hemangiomas and Other Benign Liver
glycerin (100 to 200 (g), additional heparin, small
doses of tissue plasminogen activator, and tincture
Tumors (Online Case 89)
of time usually resolve the problem. Hemangioma is the most common benign mass found
in the liver. These lesions are vascular tumors charac-
PORTAL VEIN THROMBOSIS OR terized by collections of blood spaces lined with an
STENOSIS endothelium223 (see Chapter 1). They are usually small
Significant portal vein (PV) stenosis or thrombosis is (' 3 cm in diameter), may be multiple, and are more
uncommon (up to 7% of pediatric recipients; 1% to 3% common in women than men. Hemangiomas often are
of adults).185,198,209 At sonography, PV obstruction is sig- silent, although the mass can cause abdominal pain
naled by absence of flow, focal areas of stenosis with or hemorrhage. On CT imaging, hemangiomas show
increased peak velocity, or alterations in normal flow peripheral enhancement in the arterial phase of con-
patterns and phasicity.210 Contrast CT usually depicts trast injection, with gradual fill-in through the portal
the lesion convincingly (Fig. 12-38). When repair is indi- and equilibrium phases (Fig. 12-41). On MRI, they
cated, direct catheter-based pressure measurements have a similar pattern and are intensely bright on T2-
confirm the significance of the narrowing ($5 mm Hg). weighted and gadolinium-enhanced images.224-226 The
Stenoses respond extremely well to angioplasty and angiographic appearance is almost pathognomonic,
selective stent placement.211,213 However, the majority of with a normal-caliber feeding artery, absence of neo-
thrombotic obstructions require operative repair.192 vascularity, and pooling of contrast in amorphous
396 III. VISCERAL ARTERIES AND VEINS
A B
C D
E
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 397
spaces (see Fig. 12-41). Contrast puddles linger well is often recommended for two reasons: (1) the risk for
into the venous phase of the arteriogram because rupture (particularly when the tumor is greater than
of slow flow in the lesion. These features differen- 4 to 5 cm), and (2) the rare possibility for malignant
tiate hemangioma from hepatocellular carcinoma. degeneration.231 Prophylactic or urgent endovascular
Although surgery is rarely indicated, transcatheter embolotherapy has also been employed in small series
embolization is done preoperatively for large, symp- of patients, with tumor regression observed in most
tomatic masses and emergently for actively bleeding cases.230,232
ones.227-229 Focal nodular hyperplasia is another uncommon benign
Hepatic adenoma is a rare benign liver tumor that is hepatic mass with demographic pattern and imaging
largely a disease of young to middle-aged women who features similar to hepatic adenoma. Symptoms usually
take oral contraceptives. Other associations included arise from mass effect causing abdominal pain. On imag-
androgen hormonal therapy in men and glycogen stor- ing studies, a central scar or septations are fairly specific.
age diseases.230 Most patients are asymptomatic. Cer- While operative resection is the treatment of choice in
tain imaging findings are characteristic, but distinction most patients, embolization has been effective in selected
from other liver lesions may be problematic. Resection individuals.233,234
A B
C D
FIGURE 12-38 Liver transplant portal vein occlusion. A, Color Doppler ultrasound demonstrates high-velocity jet with turbulent flow
at the portal vein anastomosis. B, Reformatted coronal contrast-enhanced CT shows the likely obstruction (arrow). C, A right portal vein
radicle was punctured from the midaxillary line. D, Transhepatic portography reveals progression to total occlusion. Continued
398 III. VISCERAL ARTERIES AND VEINS
E F
G H
FIGURE 20-38, contd Total occlusion traversed with an angled glidewire (E). Central portography shows a large coronary vein (arrows).
The varices were embolized with coils, and the portal vein dilated with a 10-mm balloon. Although the technical results look good (F), repeat
CT scanning about 4 months later showed reocclusion. This time, with a transjugular intrahepatic approach, the diseased portal vein was
reentered (G). Embolized varices remain obstructed, but new ones are developing (arrow). Balloon-expandable stents were placed across the
portal vein anastomosis (H).
A B
E F
400 III. VISCERAL ARTERIES AND VEINS
FIGURE 12-40 Posttransplant hepatic artery aneurysm. Celiac arteriogram shows a large bilobed aneurysm at the transplant arterial
anastomosis. The etiology is not clear.
Marked elongation, tortuosity, and calcification of the nodosa, numerous intrahepatic or intrasplenic microan-
splenic artery is a frequent finding in older patients. eurysms are characteristic (Fig. 12-45).
Atherosclerosis may progress to complete thrombotic Although the natural history of some visceral aneu-
occlusion (Box 12-16). However, the extensive collateral rysms is one of slow growth and eventual rupture, it is
pathways to the spleen and the dual blood supply of the difficult to predict which ones will ultimately leak.
liver usually prevent organ infarction. Splenic infarction Hemorrhage may occur into the peritoneal space, lesser
is generally the result of hematologic disorders or acute sac (splenic aneurysms), or biliary system (hepatic aneu-
embolization (usually from the heart)245 (Fig. 12-43). Dis- rysms). The following indications for treatment are fairly
section of the hepatic or splenic artery may be posttrau- well established:
matic (iatrogenic) or spontaneous (e.g., extension of a
celiac artery dissection)246,247 (see Fig. 3-25). Based on several large natural history studies,
asymptomatic dysplastic splenic artery aneurysms
larger than 2 cm in diameter warrant repair.251,253,254
Aneurysms (Online Cases 7 and 47) No clear size cutoff has been established for
The splenic and hepatic circulations are the most com- treating dysplastic hepatic artery aneurysms.255-257
mon sites for visceral artery aneurysms.248,249 True vis- Aneurysm leak with exsanguinating hemorrhage
ceral artery aneurysms are rare. They are usually small is more common with extrahepatic aneurysms;
and asymptomatic when detected, and slow-growing therefore most authorities favor early repair in
but lethal when they do rupture.248,250,251 Visceral artery almost all cases.
pseudoaneurysms are slightly more common and typi- All symptomatic or rapidly expanding true
cally symptomatic at presentation.249,252 The causes are aneurysms are repaired.
myriad (Box 12-17). The pathogenesis of dysplastic vis- Visceral aneurysms in pregnant women are
ceral aneurysm is not well understood. Women are especially prone to rupture.253,258 Fetal and
afflicted more often than men. Patients with splenic maternal mortality exceed 75%, so all visceral
artery aneurysms may have abdominal pain or hypo- artery aneurysms in women of childbearing
tension from bleeding. Hepatic artery aneurysms can potential deserve treatment.259
cause abdominal pain, hemobilia, or jaundice. Most experts endorse repair of all visceral artery
On noninvasive studies, a focally enlarged, enhancing pseudoaneurysms based on their unpredictable
vessel is seen (Fig. 12-44). Fluid or soft tissue adjacent growth pattern and high mortality rates when
to the lesion suggests an inflammatory pseudoaneurysm. they leak.249
At catheter angiography, dysplastic visceral artery Because of the excessive risk of rupture of visceral
aneurysms are often saccular, sometimes multiple, and aneurysms in patients with portal hypertension,
may be calcified. Hepatic artery aneurysms usually are these lesions are treated in candidates for or
solitary and extrahepatic. In patients with polyarteritis recipients of liver transplant.260
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 401
A B
C D
E F
FIGURE 12-41 Cavernous hemangioma of the liver. Arterial phase (A and B) and slightly delayed (C and D) CT scans show two huge
hypodense masses in the right and left liver lobes with nodular peripheral enhancement that migrates centrally and persists into the later phase.
E and F, Early and later phase of celiac arteriogram demonstrate huge masses occupying large parts of the liver with innumerable contrast puddles
that remain in the venous phase of the study. Note the normal-caliber hepatic artery and lack of any hypervascularity or neovascularity.
Transcatheter embolization is the treatment of vessels feeding the distal artery (closing the back
choice for most intrahepatic and splenic artery aneu- door). Even with properly performed large vessel em-
rysms and pseudoaneurysms.248,249,261 The preferred bolotherapy, about 40% of patients treated for splenic
embolic agent is a coil; Gelfoam pledgets can be used artery aneurysms will suffer partial or complete
to accelerate thrombosis. When feasible, embolization splenic infarction (which may be quite symptomatic)
across the aneurysm neck is important to prevent de- or pancreatitis.252,262,263 If the parent artery allows de-
layed retrograde flow into the sac through collateral livery of an appropriately sized sheath, covered stent
402 III. VISCERAL ARTERIES AND VEINS
C AU S E S O F C AU S E S O F H E PAT I C A N D
A RT E R I O V E N O U S S P L E N I C A RT E RY
SHUNTING IN THE LIVER NARROWING
Vasculitis
Several forms of arteritis are seen in the liver and spleen.
Polyarteritis nodosa and illicit drug use can produce a
necrotizing vasculitis that may involve the liver,
FIGURE 12-42 Vascular ectasias of the liver and stomach on kidneys, intestinal tract, and extremities (see Fig. 12-45).
celiac arteriography (arrows) in a patient with hereditary Liver involvement with giant cell arteritis also has been
hemorrhagic telangiectasia. described.265
Hypersplenism
placement is a better alternative to exclude the aneu-
rysm but maintain vessel patency.264 In hypersplenism, the physiologic destruction of cellu-
Surgery (by exclusion, excision, or bypass grafting) lar blood elements by the spleen is exaggerated be-
is required for some extrahepatic artery aneurysms cause of reticuloendothelial hyperplasia in the organ.
and for failures of embolotherapy. Rarely, splenic artery The syndrome is associated with cirrhosis and portal
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 403
A C
B
FIGURE 12-43 Celiac artery embolism. A, Transverse contrast-enhanced computed tomography (CT) scan shows lack of opacification
of the celiac axis, which is confirmed on a sagittal reformatted image (B, arrow). C, CT scan shows splenic infarction because of the acute
ischemic insult.
BOX 12-17
C AU S E S O F S P L E N I C A N D H E P A T I C A R T E R Y
A N E U RY S M S A N D P S E U D O A N E U RY S M S
A B
C
12. HEPATIC, SPLENIC, AND PORTAL VASCULAR SYSTEMS 405
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C H A P T E R
13
Endocrine, Exocrine, and Reproductive
Systems
Karim Valji
412
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 413
Gastroduodenal artery
Posterior
superior
pancreatico-
duodenal
artery Dorsal pancreatic artery
Anterior
superior
pancreatico-
duodenal
artery
A B
Right gastroepiploic artery Pancreatic Transverse
head arcades pancreatic artery
FIGURE 13-1 Pancreatic arterial anatomy. A, Gastroduodenal arteriogram. B, Dorsal pancreatic arteriogram from the undersurface of the
celiac artery.
pancreatectomy, and palliative diversion for biliary Somatostatinomas are associated with gallstones,
obstruction (i.e., choledochojejunostomy) or duodenal diabetes, and weight loss.
obstruction (i.e., gastrojejunostomy). Preoperative or Nonfunctioning tumors (some of which
postoperative adjuvant radiation therapy and chemo- release pancreatic polypeptide or other obscure
therapy are used in some centers.14,15 hormones) cause symptoms by mass effect
(jaundice, abdominal pain) and are, therefore,
Pancreatic Neuroendocrine quite large at presentation. They usually are
(Islet Cell) Tumors solitary and malignant but slow growing.
A B
FIGURE 13-2 Glucagonoma. A computed tomography scan (A) and late phase splenic arteriogram (B) show a hyperdense mass in the tail
of the pancreas (arrow).
Inflammatory Diseases
Etiology and Clinical Features
Acute pancreatitis is the consequence of autodigestion
of the gland after release of proteolytic enzymes into
itself.47 An intense inflammatory reaction ensues, leading
to hemorrhage and fat necrosis. If the patient survives
the acute episode, the disease can progress to phlegmon,
abscess, or pseudocyst formation, any of which may
FIGURE 13-3 Gastrinoma. Computed tomography arteriogram spread widely throughout the abdomen or pelvis.
with contrast injection into the celiac artery shows a densely Chronic pancreatitis follows repeated bouts of acute pan-
enhancing mass adjacent to the duodenum and pancreatic creatitis or chronic pancreatic duct obstruction and is
head (arrow). characterized by diffuse fibrosis, gland calcification, and
pseudocyst formation.
In the United States, the most common risk factors for
insulinoma or gastrinoma (respectively) to liberate large acute and chronic pancreatitis are alcohol abuse and
quantities of hormone. Blood samples are obtained soon biliary tract obstruction (e.g., gallstones). Other causes
thereafter for hormonal analysis from the hepatic veins, include trauma, surgery, biliary cirrhosis, infection,
which ultimately drain most islet cell neoplasms. A sig- drugs, hyperparathyroidism, and hyperlipidemia. Acute
nificant step-up compared with peripheral venous levels pancreatitis can become a medical emergency with se-
will localize the lesion to the vascular territory of the vere abdominal pain and shock. Both serum amylase
injected artery. In experienced hands, arterial stimu- and lipase levels are helpful in diagnosis.
lation with venous sampling is close to 100% accurate Vascular complications follow about 10% of cases
in preoperative detection of gastrinomas and insulin- of severe pancreatitis.48-50 They include splenic or portal
omas.31-38 vein thrombosis, pseudocyst hemorrhage, formation
of small intrapancreatic or large vessel pseudoaneu-
Treatment rysms from enzymatic destruction or severe inflamma-
Standard management of solitary, localized pancreatic tion, and pseudoaneurysm rupture. Blood may leak
neuroendocrine tumors is surgical resection.17,18,20 Nonop- into the peritoneal cavity, retroperitoneum, or gastroin-
erable individuals are relegated to medical therapy, which testinal tract (directly into bowel or via the biliary
416 III. VISCERAL ARTERIES AND VEINS
A B
FIGURE 13-4 Insulinoma. A, A region of hypervascularity in the pancreatic head is identified by celiac arteriography (arrow). B, After
intraarterial injection of 1 mEq of calcium gluconate, the islet cell tumor is readily seen during gastroduodenal artery injection.
system [hemosuccus pancreaticus]). Thus, hemorrhage is damaged artery through collateral channels (Fig. 13-6).
signaled by gastrointestinal blood, falling hemoglobin, Embolization generally is safe in the upper gastrointes-
or hypotension. In a patient with a history of pan- tinal tract. Occlusion of small or large bowel branches
creatitis, erosion of a pseudoaneurysm or pseudocyst (e.g., jejunal arteries, middle colic artery arising from
into the portal vein can produce hyperdynamic portal the dorsal pancreatic artery) poses some risk of bowel
hypertension. infarction. Permanent control of hemorrhage is achieved
in about 75% of attempts.53-56 However, a significant
Imaging number of patients require second-look angiography
Vascular sequelae of pancreatitis are first identified by to identify new bleeding sites.57 Even with aggres-
CT, sonography, or (less often) MRI.51,52 Arteriography sive coordinated multispecialty care, mortality is still
is exclusively reserved for patients with a suspected substantial.
vascular event who may require endovascular inter-
vention. Large pseudoaneurysms, bleeding pseudo-
cysts, and free extravasation are readily seen on CT OTHER DISORDERS
and angiography (Fig. 13-5). A thorough search for the
culprit lesion may require angiography of the splenic,
Pancreas Transplant Complications
hepatic, gastroduodenal, dorsal pancreatic, and pancre-
aticoduodenal arteries. Transplantation of the pancreas (often combined with
kidney grafting) is performed for selected patients with
Treatment type 1 diabetes. In one operative approach, the donors
Embolization is the optimal treatment for most hemor- iliac artery is harvested along with the pancreas and its
rhagic complications of pancreatitis, particularly because arterial supply from the splenic artery and SMA. Off
many of these patients are very poor surgical candi- the operating field, the transplant splenic artery and
dates53-57 (see Fig. 13-5). The most sensible approach SMA are connected to the internal and external iliac
is endovascular deposition of coils and Gelfoam pled- artery stumps, respectively.59 The common iliac artery
gets. Occasionally, other materials and routes are used, trunk of the resulting Y-graft is then anastomosed
including direct percutaneous thrombin injection.58 to the recipients external iliac artery (Fig. 13-7). The
Blockade across the neck of a pseudoaneurysm is neces- donor portal vein is connected to the recipient external
sary to prevent backfilling from the distal segment of the iliac vein.
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 417
A B
C D
FIGURE 13-5 Pancreatic pseudocyst causing upper gastrointestinal bleeding. A, Contrast-enhanced computed tomography scan shows
a huge hypodense mass occupying the retroperitoneal space surrounded by pancreatic tissue. A percutaneous drain was subsequently placed.
Several days later, massive upper intestinal bleeding occurred. B, Celiac arteriogram shows the hemorrhage from the gastroduodenal artery
(arrow). Profound constriction of all celiac branches is because of shock. C, Microcatheterization of the bleeding vessel was done, followed
by microcoil and Gelfoam embolization. D, The artery is obstructed (arrow), and bleeding has ceased.
A B
A B C
FIGURE 13-7 Pancreas and kidney transplant. A, Pelvic angiography shows the right external iliac artery anastomosis to the pancreas
(large arrow) and left external iliac artery connection to the kidney (small arrow). Early (B) and late (C) selective pancreatic arteriography shows
the vascular anatomy and opacification of the entire gland.
A B
FIGURE 13-8 Bilateral adrenal vein sampling for hyperaldosteronism. Patient had difficult-to-control hypertension and right adrenal
adenoma on CT imaging. A, Left adrenal venography (arrow) at the origin of the phrenicoadrenal trunk. B, Right adrenal vein has a delta
configuration. Hormonal assay showed bilateral adrenal hyperplasia (see Table 13-3).
420 III. VISCERAL ARTERIES AND VEINS
A B C
E F
FIGURE 13-9 Bilateral adrenal vein sampling for hyperaldosteronism with aberrant anatomy. Patient had difficult-to-control hypertension.
A, Computed tomography scan shows large right adrenal mass (arrow). B, Catheterization of a small hepatic vein. Note homogenous liver
stain. C, Right adrenal venography. The left renal vein could not be easily found. D, Computed tomography scan shows presence of retroaortic
left renal vein (arrow). This vein was catheterized (E), and the adrenal vein sampled (F). Hormonal assay proved active aldosteronoma
(see Table 13-4). This was confirmed at operation.
MAJOR DISORDERS
Cushing Syndrome
TABLE 13-1 Causes of Hypercortisolism
Hypercortisolism has several causes77 (Table 13-1).
Benign adenomas tend to be small, but functioning adre- ACTH DEPENDENT (ABOUT 80% OF CASES)
nal carcinomas often are quite large at the time of presen-
Pituitary adenoma (Cushing disease)
tation. Cushing syndrome occurs in both adults and Ectopic cortisol-releasing hormone tumor
children.77 Patients classically suffer from hypertension,
hirsutism, abdominal striae, obesity, diabetes, and men- ACTH INDEPENDENT (ABOUT 20% OF CASES)
tal disturbances. By definition, the serum cortisol level Adrenocortical adenoma
is elevated. A high-dose dexamethasone suppression test Bilateral adrenal hyperplasia
will discriminate between adrenocorticotropin hormone Adrenal carcinoma
Excess cortisol intake
(ACTH)dependent adrenal hyperplasia from a pituitary
tumor and an ACTH-independent adrenal tumor. ACTH, adrenocorticotropin hormone.
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 421
If a pituitary mass is found, inferior petrosal sinus sam- TABLE 13-3 Adrenal Vein Sampling after Cortrosyn
pling confirms the corticotropin gradient and is often Stimulation Results for Figure 13-8
requested before operative removal.78 Otherwise, an Aldosterone/
adrenal mass is sought with sonography, CT, MRI, or Site Aldosterone Cortisol Cortisol Ratio
radionuclide-based PET/CT.79-82 If routine imaging
Right adrenal vein 960 428 2.2
studies are nondiagnostic, adrenal venous sampling Left adrenal vein 1300 648 2.0
should be performed.34 A unilateral cortisol gradient is Inferior vena cava 21 26 0.8
diagnostic of adrenal adenoma or adenocarcinoma.83
The preferred therapy is adrenalectomy.
TABLE 13-4 Adrenal Vein Sampling after Cortrosyn
Stimulation Results for Figure 13-9
Aldosteronism (Video 13-1)
Aldosterone/
Etiology and Clinical Features Site Aldosterone Cortisol Cortisol Ratio
Primary aldosteronism has several causes84 (Table 13-2). Right adrenal vein 1800 302 6.0
In the past, aldosteronism was reported as the cause for Left adrenal vein 430 804 0.5
hypertension in about 1% to 2% of the general popula- Inferior vena cava 74 37 2.0
tion. However, new evidence supports a higher preva-
lence (5% to 13%) even among unselected groups.85-88
A hyperfunctioning adrenal adenoma is the culprit in scans can be extremely helpful in identifying the precise
about 35% of cases.87-89 These adenomas tend to be location of the right adrenal vein connection with the IVC.
smaller (&2 cm) than those seen with Cushing syndrome. The technique for adrenal vein sampling is described ear-
Secondary aldosteronism usually is a consequence of lier. Blood aliquots are obtained from the right and left
renal artery stenosis, which elevates renin levels and acti- adrenal veins and from the IVC for aldosterone and corti-
vates the renin-angiotensin-aldosterone system. sol analysis. High cortisol levels confirm that the correct
Patients with primary or secondary aldosteronism are vein was catheterized. Many experts believe that sampling
hypertensive. Hypokalemia, metabolic alkalosis, and should be done after (and possibly before) ACTH stimula-
elevated urinary aldosterone metabolites are character- tion with cosyntropin (Cotrosyn 250 'g IV). In fact, it is the
istic. A serum aldosterone/renin ratio greater than 20 to relative suppression of aldosterone from the uninvolved
25 is often used as a threshold for further investigation.90 gland that is most predictive of a positive outcome from
surgery.93 An aldosterone/cortisol ratio from the sus-
Imaging pected side more than four to five times greater than the
The distinction between a functioning tumor and bilat- ratio in the contralateral vein is diagnostic (Tables 13-3 and
eral adrenal hyperplasia is essential, because the former 13-4 and see Figs. 13-8 and 13-9). Sequential (rather than
is treated with surgery or ablation for cure and the latter simultaneous dual catheter) sampling does not appear to
is treated medically with aldosterone antagonists. CT, diminish accuracy despite normal temporal fluctuations
MR, and radionuclide-based PET/CT are the primary in hormone release.92
imaging options for lesion detection. However, non-
functioning adrenal adenomas (incidentalomas) are Treatment
commonly detected on CT and MR and can be mistaken Bilateral hyperplasia is managed with drug therapy. Spi-
for a functional aldosteronoma.91 ronolactone (Aldactone) is a particularly effective competi-
Adrenal venous sampling is essential to establish with tive inhibitor of aldosterone activity in the renal tubules.
near certainty that a suspicious adrenal lesion is the cul- Functioning adenomas and adrenal carcinomas are
prit.34 In one recent report, CT or MRI mistook a nonfunc- treated by open adrenalectomy or laparoscopic techniques.
tioning adrenal adenoma for a functioning tumor in 38% The evidence to support percutaneous ablation by arterial
of cases before classification with venous sampling.91 embolotherapy (e.g., with alcohol sometimes admixed
Among experienced practitioners, sampling is accurate in with contrast material) or RFA is only anecdotal.94-96
more than 90% of attempts.89,92,93 Novices should not ini-
tially expect such reliable outcomes. High-quality CT
OTHER DISORDERS
TABLE 13-2 Causes of Hyperaldosteronism
ovary syndrome and certain ovarian neoplasms are rarely procedure.34,105 A complete study requires selective
associated with excess testosterone production. Virilizing catheterization of inferior, superior, and middle thyroid
adrenal tumors typically release dehydroepiandrosterone veins along with the thymic and internal jugular veins.
(DHEA) and dehydroepiandrosterone sulfate.97 Urinary Central large vein sampling (i.e., bilateral internal jugu-
17-ketosteroid levels are markedly elevated in either situ- lar and brachiocephalic veins) is simpler but may be
ation. Affected women complain of hirsutism, menstrual less accurate.106-108 Small contrast injections are made
dysfunction, acne, and obesity. after obtaining blood aliquots to document catheter
CT, transvaginal sonography, or MRI is recommended position. In postoperative patients, the vertebral veins
for evaluation of this vexing clinical problem. If the results also are sampled at several sites.
are equivocal, bilateral adrenal and ovarian venous sam-
pling should be performed.98 Various hormonal levels
are measured, including testosterone, DHEA, and andro- ANATOMY
stenedione. Virilizing adrenal or ovarian tumors are dis-
tinguished by the abnormally high hormone ratio between The primary routes of venous drainage from the normal
the ipsilateral vein and a peripheral blood sample. parathyroid glands are as follows:
Inferior thyroid vein to the upper surface of the
Pheochromocytoma left brachiocephalic or right internal jugular vein
Superior and middle thyroid veins to the internal
Rare tumors of chromaffin cells of the sympathetic
jugular vein
nervous system originate in the adrenal medulla (pheo-
Thymic vein to the undersurface of the left
chromocytoma) or extraadrenal sites (paraganglionomas or
brachiocephalic vein
chemodectomas).99 The disorder is tagged with the 10%
rule, whereby 10% of lesions are extraadrenal, meta- During surgery for parathyroid disease, the thyroi-
static, bilateral, cystic, or associated with MEN-2 syn- dal veins often are ligated.109 The thyroid bed then emp-
drome. In fact, the likelihood of ectopic location and ties through collateral channels that join the vertebral
malignancy varies with the existence of inherited links veins.
to the disease.100 Almost a third of affected individuals
(including sporadic cases) have an identifiable genetic
defect. Symptoms are related to excess production of MAJOR DISORDERS
catecholamines (including epinephrine and norepineph-
rine) in addition to other hormones from the pathologic Hyperparathyroidism
tissue.
The diagnosis of pheochromocytoma or paragangli- Etiology and Clinical Features
onoma usually is made with metaiodobenzylguanidine Primary hyperparathyroidism is a disorder of excess
scintigraphy, MRI, or CT scanning.101 Iodinated contrast secretion of parathyroid hormone (PTH) from solitary or
material given by any route may precipitate a poten- multiple parathyroid adenomas, bilateral gland hyper-
tially lethal hypertensive crisis.102 Patients with sus- plasia, or parathyroid carcinoma.110 Adenomas account
pected pheochromocytoma should be pretreated with for about 80% of cases. Patients with either MEN-1 or
alpha-adrenergic and possibly beta-adrenergic antago- MEN-2 may suffer from active parathyroid adenomas.100
nists. A typical regimen includes phenoxybenzamine for The resulting hypercalcemic state is responsible for
several days before the procedure (20 mg orally twice kidney stones, abdominal pain, renal dysfunction, and
daily) and phentolamine (5 to 15 mg IV) as needed during dehydration seen in this disease. Conventional man-
the procedure. agement entails surgical resection of the offending
CT-guided RFA or percutaneous ethanol injection adenoma or subtotal parathyroidectomy for glandular
(PEI) have been employed on occasion for treatment of hyperplasia. In a few individuals, symptoms persist or
these lesions.96,103 recur after surgery because of ectopic or supernumerary
glands or incomplete removal of hyperplastic tissue.
Residual tumors usually are found in the tracheoesoph-
PARATHYROID GLANDS ageal groove of the superior mediastinum, in the thy-
mus, or within the thyroid gland.
ANGIOGRAPHY
Imaging
Parathyroid arteriography is a procedure of the Patients with hyperparathyroidism are first evaluated
past.104,105 Parathyroid venous sampling is still done on with the most sensitive imaging modalities avail-
rare occasions, and it can be a demanding and complex able, namely sonography (with or without fine-needle
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 423
aspiration of detected masses for PTH levels), 99mTc- vein is diagnostic of excess hormone production from
sestamibi scintigraphy, or 11C-methionine PET/CT the drained site. If symptoms persist after surgery or
of the neck and mediastinum.111-115 When two studies parathormone levels remain elevated, reoperation is
are positive for a solitary adenoma, most surgeons usually preceded by a more aggressive workup, espe-
proceed with removal. CT and MRI are second-tier cially selective venous sampling (Fig. 13-10).116-118 In
imaging options. If detection remains elusive, selective one large contemporary series, ectopic glandular tis-
parathyroid venous sampling may be diagnostic.108 A sue was found in close to one third of reoperations for
2:1 PTH ratio between a sampled site and a peripheral disease.113
A B C
D
FIGURE 13-10 Venous sampling for recurrent hyperparathyroidism. A, Samples for parathormone assay are obtained at various levels
of the right internal jugular (IJ) vein B, Left internal jugular vein via a collateral (central IJ vein is obstructed, arrow). C, Right middle thyroid
vein. D, Inferior thyroid vein.
424 III. VISCERAL ARTERIES AND VEINS
Treatment
Minimally invasive surgery (sometimes with intraop-
erative sonography) is preferred by many experienced
operators.119 The recent availability of ultrarapid PTH
assay now makes intraoperative hormone analysis
practical in guiding open or laparoscopic parathy-
roid resection.107 Reoperation is curative in greater
than 90% of cases when a robust imaging sequence is
followed.112,113,117,120
Transcatheter arterial ablation of residual parathyroid
adenomas has been described.117,121 Injection of absolute
alcohol is usually sufficient to destroy the lesion. The
procedure should be performed only if some parathy-
roid tissue is preserved to prevent hypoparathyroidism.
FIGURE 13-11 Right internal pudendal arteriogram in a patient
MALE REPRODUCTIVE SYSTEM with peroneal trauma and possible arteriocavernosal fistula causing
priapism. The cavernosal artery is truncated beyond its origin. Staining
of the bulb of the corpus spongiosum is normal. B, artery to the bulb;
ARTERIOGRAPHY AND VENOGRAPHY C, cavernosal artery; CPA, common penile artery; D, dorsal penile
artery; IPA, internal pudendal artery; S, scrotal branches.
A B
FIGURE 13-12 Normal cavernosography. A, Both corpora cavernosa are filled to the crura (arrows), and the deep dorsal vein is filled.
B, The intercavernosal septum (arrow) is seen in another patient. The cavernosa drain into the preprostatic plexus and then into internal
pudendal and other deep pelvic veins.
MAJOR DISORDERS
Male Varicocele
Etiology
Varicocele is a dilation of the pampiniform plexus in
the scrotum with or without central venous dilation.126
The disorder affects about 15% of the general adult
male population.127 Most cases occur on the left side
of the body. The right side is involved in up to 10% of
affected men, although some reports note a much
higher frequency.128,129
The origin of primary varicocele is debated.126,130,131
Various theories have been proposed, including ab-
sence or abnormal formation of internal spermatic
vein valves and compression of the left renal vein,
causing internal spermatic vein hypertension. Regard-
less of the cause, venous reflux and chronic venous
hypertension are the result. Secondary varicocele is
caused by abdominal or pelvic masses that impede
drainage of the pampiniform plexus. The sudden on-
set of varicocele in an older man or the presence of
a right-sided varicocele should raise the suspicion of
a neoplasm (e.g., left renal vein invasion from renal
cell carcinoma).
FIGURE 13-13 Right gonadal venogram. The vein is dilated and
shows significant reflux. Clinical Features
Although more than 80% of patients with varicocele are
asymptomatic and do not have a specific problem with
cases.125 Important anomalies include drainage of the fertility, the remainder can suffer from scrotal pain and
right internal spermatic vein into the right renal vein swelling.132 Up to 40% of men evaluated in infertility
(8%) and multiple terminal gonadal veins (15% to clinics are found to have a varicocele.133 The explanation
20%). Valves are present in most but not all internal for diminished fertility in this population is controver-
spermatic veins. sial. The leading hypotheses invoke elevations in scrotal
426 III. VISCERAL ARTERIES AND VEINS
temperature or backflow of renal or adrenal metabolites inguinal ring (Ivanissevitch procedure), or subinguinal
as a cause for testicular dysfunction and suboptimal level (Marmor procedure). Laparoscopic varicocelec-
sperm production or function. As such, abnormalities of tomy is favored by many surgeons.136,137
total sperm count, sperm density, and sperm motility are
found in many patients with varicocele. VARICOCELE EMBOLIZATION
Technique A diagnostic venogram on the affected
Imaging side is obtained to document valvular incompetence,
Most varicoceles can be detected by physical exami- reflux of contrast, venous dilation, and filling of collat-
nation alone. When the diagnosis is equivocal or a eral tributaries (see Fig. 13-13 and Fig. 13-14). Catheter-
subclinical varicocele is suspected (i.e., infertility with ization of the gonadal veins may be difficult if variant
abnormal sperm activity but a nonpalpable varicocele), anatomy is present.138 The preferred obliterative mate-
the scrotum is evaluated with duplex sonography.134 rial is coils with or without adjuvant sclerosing agent
Spermatic venography is reserved for patients under- such as 3% sodium tetradecyl sulfate foam. Cyanoacry-
going embolotherapy. lates (glue) and polidocanol are alternative agents.139-143
The internal spermatic vein is first occluded at the level
Treatment of the superior pubic ramus. Material is then deposited in
The commonly (but not universally) accepted indica- stages up to the vein origin, taking care not to allow coil
tions for invasive varicocele obliteration are scrotal springs to extend into the renal vein or IVC. Venography
pain, massive size, testicular hypoplasia in adolescent is repeated periodically to identify collateral channels that
boys, and infertility with laboratory evidence for sperm also may require obliteration. Nitroglycerin (100 to 200 'g)
dysfunction.* is given to relieve venospasm. In patients with solitary
left-sided varicocele, right-sided embolization is performed
SURGICAL THERAPY only when the right internal spermatic vein is incompetent
Operation for varicocele entails surgical interruption of and the goal is improved fertility.
the internal spermatic vein and collateral vessels. Classi- Results Embolotherapy is technically successful in
cally, ligation is performed at the retroperitoneal, internal more than 90% of cases.139-150 No particular embolic
agent or combination has proven most effective. The
*See references 126, 127, 129, 130, 132, 135. usual reasons for initial failure are inability to cannulate
A B
FIGURE 13-14 Varicocele embolization. A, Selective catheterization of the lower left internal spermatic vein about the inguinal ligament.
Several platinum coils and Gelfoam pieces were placed. Because several collateral channels opacified, sodium morrhuate was injected as a
liquid sclerosant. B, Additional platinum coils separated by Gelfoam pieces were deposited along the course of the vein up to its orifice at the
left renal vein.
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 427
the internal spermatic vein or traverse a competent remains well oxygenated. The fistula can be confirmed
valve, venospasm, and the presence of multiple central with angiography and obliterated by superselective
collateral veins. Pain relief is almost invariable.141 The embolization of the cavernosal arteries with either tem-
late recurrence rate is 4% to 12%, primarily because of porary (e.g., Gelfoam) or permanent agents (e.g., coils
the development of collateral channels.141,145,148,151 Over- or small particles) (Fig. 13-15). Resolution of priapism
all, results of embolotherapy are comparable to surgery and maintenance of normal erections is the rule, but
and excellent after failed surgical ligation.152-156 One recurrence rates are significant.166-169
study found that duplication of the gonadal vein deep When imaging for potentially treatable vascular
in the pelvis was a common finding in men with recur- causes of erectile dysfunction seems necessary, duplex
rent or persistent varicocele after operation who were sonography is the best option. Angiography has no role
referred for embolotherapy.139 unless a post-traumatic arteriovenous fistula is sus-
At present, the value of embolotherapy or surgery for pected or surgical bypass is being considered in a rela-
varicocele in infertile men is being contested. Early re- tively young patient.
ports claimed significant improvement in sperm density
and motility in most cases; about one fourth to one
third of couples become pregnant in follow-up studies.* FEMALE REPRODUCTIVE
Recent studies have failed to show increased likelihood
of pregnancy or association of pregnancy with improved
SYSTEM
sperm quality after varicocele embolization.158,159 In fact,
aggregate analysis of reported randomized trials of ANATOMY
treated versus untreated infertile men failed to identify
any benefit from varicocele embolization in this re- The ovaries are fed by the ovarian arteries, which exit the
gard.160 Still, many practitioners dispute this wholesale anterolateral surface of the aorta below the renal arteries
rejection of these methods.131,135 (see Fig. 7-1). The vessels descend into the pelvis and
Complications Minor flank or scrotal pain, low- then enter the broad ligament of the uterus. The right
grade fever, and transient numbness over the anterior ovarian vein empties directly into the IVC below the right
thigh are minor side effects of the procedure. Vein rup- renal vein. The left ovarian vein drains into the undersur-
ture with extravasation usually is self-limited. Adverse face of the left renal vein. Variant anatomy is seen in a
events specific to embolotherapy are uncommon (5% to minority of cases.170
10%) and include migration of coils to the lung, throm- The uterus is primarily supplied by the uterine arter-
bosis of the pampiniform plexus, and aspermia.136 ies, which usually take off as separate branches of the
anterior divisions of the internal iliac arteries.170 They
course medially in the broad ligament and then ascend
OTHER DISORDERS along the lateral border of the uterus. These vessels have
anastomoses with branches of the ovarian arteries (see
later discussion).
Trauma
Direct penile injury can be caused by blunt or penetrating
trauma or during sexual activity (e.g., penile fracture). MAJOR DISORDERS
Potential sequelae include penile deformity, urethral dam-
age, or impotence.161-163 Cavernosography may be re- Uterine Leiomyomas (Fibroids)
quested to delineate the damage to the corpora cavernosa (Online Case 21 and Video 13-2)
and venous drainage (see earlier discussion).
Priapism refers to sustained penile erection without Etiology
direct stimulation or sexual desire. Low-flow priapism is Uterine leiomyomas (fibroids) are the most common tumor
caused by sludging of blood in the corpora and impeded affecting the female reproductive organs and occur in
venous outflow.164,165 Corporal blood aspirates will be about 20% to 25% of all women.171 Histologically, they
relatively hypoxic. The list of precipitating factors is are benign neoplasms composed primarily of whorls of
long, but the consequence is effectively penile ischemia smooth muscle cells and fibrous stroma. These discrete
that must be relieved emergently or risk necrosis of lesions are classified by location as intramural, subserosal,
the corpora cavernosa. Blunt perineal or penile trauma or submucosal. Uterine fibroids are usually silent and do
is rarely followed by high-flow priapism from a direct not require treatment.
arteriocavernous fistula. In this case, corporal blood As the tumors enlarge, cystic degeneration and cal-
cific deposits can result. Fibroids also may become pe-
*See references 141, 142, 148, 152-154, 157. dunculated, with long stalks that allow them to migrate
428 III. VISCERAL ARTERIES AND VEINS
D
C
A B
into the cervix, vagina, or abdomen. Degeneration into they are hormonally sensitive, fibroids enlarge rapidly
leiomyosarcoma is rare but has been described. Leiomyo- during pregnancy and usually regress after menopause.
mas must be distinguished from their malignant relative Most fibroids do not produce symptoms. When they
and from adenomyosis, which refers to benign invasion of do, it is primarily by mass effect on the bladder, ureters,
endometrial gland tissue into the myometrium that and adjacent pelvic structures. Women may suffer from
causes generalized uterine enlargement. Isolated foci of pain, pressure, or heaviness in the pelvis, back, perineum,
adenomyosis also can mimic leiomyoma. or legs; heavy menstrual bleeding; abdominal bloating;
urinary frequency or incontinence; and ureteral obstruc-
Clinical Features tion.172 Submucosal fibroids can interfere with normal
Fibroids are up to three times more common in African- endometrial activity and lead to prolonged menses, infer-
American women than in Caucasian women. Most tility, or prolapse into the cervix. Other diseases (includ-
symptomatic patients are between the ages of 35 and ing gynecologic malignancies such as ovarian cancer)
50 years. Development and growth of these lesions is may cause similar symptoms; they must be excluded by
attributed to both genetic and hormonal factors. Because imaging studies or other means.
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 429
Imaging shrinkage after UAE was predicted by lower signal
Transabdominal or transvaginal sonography is sensitive intensity on T1-weighted and higher intensity on T2-
in depicting uterine fibroids and in identifying concur- weighted scans.174 Adenomyosis appears as widening
rent disease or other causes for symptoms. However, of the junctional zone with bright signals in the myome-
MRI is superior to sonography in assessing the number, trium on T2-weighted images.
size, and location of fibroids; internal architecture and
vascularity; effect on adjacent structures; and presence Treatment
of coexisting adenomyosis or other pathology. For most The choice between endovascular and operative treat-
experienced practitioners, it is the preferred study ment should be made jointly by the patient, gynecolo-
before and after uterine artery embolization (UAE). gist, and interventionalist after all available treatment
Fibroids appear as discrete round masses with hetero- modalities have been considered. Only symptomatic
geneous low signal on T2-weighted images and isoin- patients in whom other causes for disease have been
tense with myometrium on T1-weighted images.173 excluded (including a recent Papanicolaou test) should
Lesions enhance variably on T1-weighted images after undergo embolotherapy. The interventionalist or sur-
gadolinium (Fig. 13-16). In one study, favorable tumor geon is obligated to become the primary physician
A B C
D E
FIGURE 13-16 Uterine artery embolization. A, Sagittal gadolinium-enhanced magnetic resonance image shows multiple intramural and
submucosal fibroids. B, Pelvic arteriogram demonstrates bilaterally enlarged uterine arteries (arrows). C, Selective right uterine arteriography
through a 4-Fr Roberts catheter shows the hypervascular fibroids. D, Following embolization with 300- to 500-'m particles, there is stasis of
flow. E, Similar findings in the left uterine artery before embolization.
430 III. VISCERAL ARTERIES AND VEINS
caring for the patient in preprocedure consultation, hos- 700 to 900 'm).179-181 The superiority of one agent over
pital recovery, and all outpatient management. another is contested.181,182 Proximal embolization (e.g.,
with coils) is inadvisable, because collateral vessels are
UTERINE ARTERY EMBOLIZATION sure to develop and continue to feed the tumors.
First reported in 1995, UAE entails small vessel occlusion Infusion of the particulate slurry (made with diluted
of feeding arteries, which causes fibroid infarction and contrast material, see Video 3-18) is continued until
eventual shrinkage, ideally providing symptom relief.175 there is static flow in uterine artery branches (pruned-
Because of the organs naturally rich collateral circulation, tree appearance). Regardless of the location of fibroids,
normal uterine tissue remains viable in most women. bilateral embolization is necessary to prevent recruit-
Patient Selection Absolute or relative contraindi- ment of collateral vessels. Completion internal iliac
cations include pregnancy, active or recent pelvic infec- arteriograms are obtained to identify any additional
tion, gynecologic malignancy (unless palliation is the vessels feeding the tumors.
goal), uncorrectable coagulopathy, severe allergy to con- The interventionalist should be observant of variant
trast material, and prior pelvic surgery or radiation arterial anatomy and important collateral vessels.183 In
therapy.176 No guarantee should be made regarding fer- most cases, the ovarian arteries feed the fibroids
tility afterward, although pregnancy can occur follow- through anastomoses with the main uterine artery. In
ing UAE. Some interventionalists are cautious about about 10% of patients, the uterine artery is the major
treating subserosal pedunculated fibroids with relatively blood supply to the ovary, or the ovarian artery has
narrow stalks despite generally good outcomes for this significant direct communication with the fibroid184
subgroup.177 (Fig. 13-17). Of course, embolization of these vessels
Technique Gonadotropin-releasing hormones that theoretically increases the risk of ovarian infarction.
may have been prescribed as medical therapy for the This is particularly true in women who have under-
condition should be stopped at least 3 months before- gone prior pelvic surgery, had other tubal pathology, or
hand. These drugs cause uterine artery constriction have fundal fibroids.185
and can make catheterization difficult. A thorough con- A postembolization syndrome consisting of pain,
sultation with the interventionalist is crucial well be- nausea and vomiting, and low-grade fever is expected.
fore the procedure. Because pain is expected afterward, Most women are hospitalized overnight, although dis-
moderate sedation and patient-controlled analgesia are charge later in the day is possible for some individu-
used liberally. Although there is no consensus about als. Pain must be aggressively managed with IV and
prophylactic antibiotics in this setting, many practitio- then oral narcotics.186 Antiemetics are given prophy-
ners choose to use them (e.g., cephazolin, 1 g IV). Ra- lactically or as needed. Discharge medications include
diation exposure should be kept to a minimum by antiinflammatory drugs (e.g., ketorolac) and potent
limiting use of prolonged acquisition, magnifica- oral narcotics. Follow-up is done by the interven-
tion, oblique projections, and wide fields of view. Fluo- tionalist, including routine clinic evaluation at 1 to
roscopy time and air kerma dose must be measured 3 weeks after the procedure.
and recorded. Results Bilateral uterine artery occlusion is techni-
A Foley catheter is inserted. The common femoral cally successful in about 95% of attempts. Incomplete
artery is the usual access route.178 A pelvic arteriogram infarction of fibroids risks continued growth.187 Clinical
with the catheter positioned in the infrarenal abdominal success with substantial improvement in symptoms is
aorta is obtained as a roadmap. Selective catheterization seen in about 80% to 90% of women.188-192 Submucosal
of the anterior divisions of the internal iliac arteries is lesions and smaller tumors seem to respond best.193
performed with a cobra or ultralong reverse-curve (e.g., The primary reasons for failure are outlined in Box 13-3.
Roberts) catheter (see Figs. 3-15 and 13-16). Once the uter- If symptoms persists and the fibroids fail to shrink on im-
ine artery is identified and selected, angiography shows aging studies, repeat UAE (with a concerted search for
the markedly dilated spiral arteries feeding the uterus collateral vessels including the ovarian arteries) is often
along with intense hypervascularity. In some cases, the warranted (see Fig. 13-17). Clinical failure or recurrence
descending portion of the uterine artery can be engaged at 5 years is identified in about 25% of treated women.188
with the diagnostic catheter. However, vasospasm may be In two randomized multicenter studies, UAE was
a problem; coaxial placement of a microcatheter directed comparable to surgical myomectomy or hysterectomy in
well into the uterine artery is then necessary. durable symptom relief from fibroids. The EMMY trial
The preferred agents for embolization are small- observed similar quality of life outcomes between UAE
caliber particulate matter, including polyvinyl alcohol and hysterectomy in women with symptomatic fibroids.194
(PVA) particles (350 to 500 or 500 to 700 'm) or tris- The REST trial compared UAE with hysterectomy or
acryl gelatin microspheres (Embospheres, 500 to 700 or myomectomy in a similar population.195 Duration of
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 431
A B C
D E
FIGURE 13-17 Ovarian artery embolization for persistent uterine fibroids. T1-weighted (A) and gadolinium-enhanced T2-weighted
(B) parasagittal magnetic resonance (MR) images show persistent enhancing fundal fibroid (arrow) several months after bilateral uterine artery
embolization. C, Coronal MR angiogram identifies a markedly enlarged right ovarian artery feeding the pelvis (arrowheads). D, Selective right
ovarian arteriogram confirms the presence of this vessel feeding the residual fibroid. E, There is stasis of flow after embolization with polyvinyl
alcohol particles.
hospital stay was shorter in embolized patients; however, Complications Significant intraprocedure and post-
10% of subjects in that group required a second interven- procedure pain is the norm with UAE.201 The most serious
tion for initial treatment failure. The most recent report of complications after embolotherapy are intrauterine infec-
an American multicenter registry for UAE confirms the tion, uterine ischemia and necrosis, pulmonary embolism,
value of the procedure.196 Only 13% of treated individuals and expulsion of pedunculated submucosal lesions.202
ultimately required hysterectomy or myomectomy. These The overall adverse event rate is about 5%; major compli-
recent papers solidify the evidence from earlier but less cations occur about 1% of the time.203 Few women have
robust series in which symptom relief with UAE was amenorrhea or a significant decrease in follicle-stimulating
comparable to reported rates for surgery but with a hormone afterward, although this happens more often in
smaller risk for complications.197-200 older individuals.188,190,192,204 Overall, less than 2% of
432 III. VISCERAL ARTERIES AND VEINS
BOX 13-3
PELVIC CONGESTION SYNDROME
(ONLINE CASE 34)
REASONS FOR UTERINE
A RT E RY E M B O L I Z AT I O N Ovarian and pelvic vein varices increasingly are being
FA I L U R E recognized as an important cause of unexplained pelvic
pain in women of childbearing age. Hormonal and
Inability to catheterize uterine arteries hemodynamic factors are thought to be responsible
Incomplete embolization for the condition.206 In a minority of cases, compression
Presence of important collaterals (e.g., ovarian of the left renal vein between the aorta and SMA
arteries) (nutcracker syndrome) is responsible.207 Most women
Large fibroids with this disorder have borne children. Typical com-
Recanalization of embolized arteries plaints are lower abdominal or perineal pain and full-
Coexisting adenomyosis or leiomyosarcoma ness, menorrhagia, dyspareunia, bladder urgency, and
polymenorrhea.208 Pain is worse usually with prolonged
standing, after intercourse, and just before or during
menses. Superficial varicosities often erupt on the vulva
treated women require subsequent hysterectomy for any and thigh.
complications of UAE.205 Unlike male varicocele, the diagnosis requires imag-
ing studies such as MRI or color Doppler sonogra-
OTHER PERCUTANEOUS METHODS phy.207,208 A significant number of asymptomatic women,
Studies are currently underway to evaluate the effective- however, demonstrate ovarian vein enlargement on
ness of MR- and ultrasound-focused surgery to ablate imaging studies obtained for unrelated reasons.209 The
uterine fibroids. In addition, ultrasound-guided cryoab- traditional operation is gonadal vein ligation along
lation has been attempted. with obliteration of collateral pathways.210 Ovarian and
selective internal iliac vein embolization is an attrac-
Surgical Therapy tive alternative to surgery if compression of the renal
For women who still wish to become pregnant, the tradi- vein is not responsible.211-214 At MRI or contrast venog-
tional treatment is open or laparoscopic myomectomy. For raphy, incompetent ovarian vein valves, main trunk
women beyond childbearing age, hysterectomy is often dilation ((1 cm), reflux, and cross-pelvic collateral
recommended. drainage are characteristic (Fig. 13-18). The majority
A B
FIGURE 13-18 Pelvic congestion syndrome. A and B, Gadolinium-enhanced magnetic resonance venography with maximum intensity
coronal projection shows reflux down a markedly dilated left ovarian vein with numerous left-sided pelvic varicosities.
13. ENDOCRINE, EXOCRINE, AND REPRODUCTIVE SYSTEMS 433
A B C
D E F
FIGURE 13-19 Embolotherapy for pelvic congestion syndrome. A and B, Left ovarian venography shows a dilated, patulous vein with
reflux into the pelvis. C, Varices and transpelvic collaterals are evident. After embolization of the ovarian vein starting in the pelvis, the left
internal iliac vein was catheterized. Large veins contributing to the varices (D) were then embolized (E). Finally, the right internal iliac vein
was embolized (F). The right ovarian vein was relatively normal and therefore not treated.
434 III. VISCERAL ARTERIES AND VEINS
placental disorders, coexisting leiomyomas, or ectopic hysterectomy, which is often accompanied by massive
pregnancy are at particularly high risk for significant hemorrhage and significant mortality. When antenatal
blood loss. Abnormalities of placentation are classified diagnosis is made (as is usually the case), some obstetri-
as placenta accreta (penetration into the uterine wall), cians elect to have occlusion balloons placed in the
placenta increta (penetration through the myometrium), proximal internal iliac arteries preoperatively through
and placenta percreta (penetration to the serosa).218 bilateral femoral artery access. The volume of fluid
Initial management of gynecologic or postpartum needed to distend each balloon and completely obstruct
bleeding entails uterine massage, drug therapy (e.g., oxy- flow is recorded by the interventionalist, and balloons
tocin), vaginal packing, closure of lacerations, and curet- are inflated in the operating room, if necessary. However,
tage for retained products. In most cases, bleeding the evidence is mixed regarding the value of this maneu-
stops with these maneuvers. Hysterectomy is required for ver in reduced blood loss or lowered mortality.227-231
life-threatening hemorrhage that cannot be controlled by
transcatheter means.
Embolotherapy is extremely effective for most cases of OTHER DISORDERS
pregnancy-related or post-hysterectomy bleeding.219-225
The procedure begins with pelvic angiography followed
Gynecologic Tumors
by bilateral internal iliac injections. Occlusion of the
branches causing the bleeding is achieved with microcoils Women with pelvic malignancies, particularly of the
or Gelfoam pledgets (Fig. 13-20). The ovarian arteries uterus and cervix, occasionally suffer massive hemor-
should be examined if no extravasation is found from rhage from vascular invasion, after radiation therapy, or
pelvic branches. Collateral vessels (i.e., lumbar, femoral during surgery. Bleeding may be vaginal or intraabdomi-
circumflex, inferior epigastric, and inferior mesenteric nal. Embolotherapy is extremely effective in stopping
arteries) are other rare potential sources of bleeding, espe- blood loss.232,233 Because of the progressive nature of the
cially in postoperative patients. After embolization, bilat- disease, occlusions must be bilateral, and the embolic
eral internal iliac arteriography is repeated to confirm that agent must be permanent and small (e.g., PVA particles or
bleeding does not continue through collateral circulation. microspheres). Rebleeding is a common problem. The
After embolization, hemorrhage stops in almost major potential complications are pelvic organ ischemia,
every case. Complications, including pelvic abscess, skin necrosis, and nerve damage (e.g., sciatic neuropathy).
organ ischemia, and nerve damage, are reported in Hormonally active ovarian neoplasms (e.g., the viril-
less than 10% of procedures. The intervention does not izing Leydig cell tumor) may be suspected on clinical
impact fertility and subsequent pregnancy if particu- grounds. Confirmation of the activity of an identified
late or liquid agents are avoided.219,222,225,226 ovarian mass or localization of a difficult-to-find lesion
In pregnant women with abnormal placentation, the may require bilateral ovarian and adrenal venous sam-
standard operation at the time of delivery is cesarean pling (see earlier).234
A B C
FIGURE 13-20 Massive pelvic bleeding after a vaginal hysterectomy. A, The initial left internal iliac arteriogram failed to identify a
bleeding site. B, Selective injection of a small branch of the anterior division through a coaxial microcatheter shows extravasation (arrow).
C, Bleeding ceased after placement of several microcoils in the vessel.
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S E C T I O N IV
PULMONARY VASCULATURE
AND VENOUS SYSTEMS
C H A P T E R
14
Pulmonary and Bronchial Arteries
Karim Valji
A B C
443
444 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B C
C D E
14. PULMONARY AND BRONCHIAL ARTERIES 445
BOX 14-1
C AU S E S O F P U L M O N A RY
A RT E RY H Y P E RT E N S I O N
Group I
Idiopathic (primary pulmonary hypertension)
Familial
Secondary
Collagen vascular disease
Portal hypertension
HIV infection
Drugs (e.g., fenfluramine-type appetite
suppressants, illicit stimulants)
Congenital systemic to pulmonary shunt
Miscellaneous causes
Pulmonary venoocclusive disease
Pulmonary capillary hemangiomatosis
Group II
Left ventricular or atrial disease
Left heart valvular disease
Left
pulmonary
artery
Pulmonic
valve
A B
C
448 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
FIGURE 14-8 Normal left pulmonary arteriogram. A, Frontal projection. B, Left posterior oblique projection lays out lower lobe branches.
small portion of the pulmonary circulation may cause a origins. As a rule, one or two bronchial arteries supply
significant rise in pulmonary artery pressure. each lung; however, up to four arteries may supply one
side. Several patterns are commonly observed (Fig. 14-10;
see also Fig. 14-5):
Normal Bronchial Artery Anatomy
Right intercostal-bronchial trunk from the right
The bronchial arteries supply the trachea, bronchi, esopha-
posterolateral surface of the aorta
gus, and posterior mediastinum, and they also act as the
Left bronchial artery from the left anterolateral
vasa vasorum of the pulmonary arteries. These vessels
surface of the aorta
may not be visible at thoracic aortography in patients
Common right and left bronchial artery trunk
without lung disease. However, they become markedly
from the anterior surface of the aorta
enlarged and serve as an important collateral pathway in
patients with certain congenital heart diseases, chronic Rarely, a right intercostal-bronchial artery trunk gives
lung infections, lung tumors, and obstruction of pulmo- rise to a left bronchial artery. Unusual bronchial artery
nary arteries or veins.12 Bronchial artery anatomy is origins are noted in Box 14-2.
extremely variable.13-15 Anatomic and angiographic stud- Bronchial arteries may have branches to the anterior
ies differ in the reported pattern and distribution of their spinal artery, which supplies the ventral portion of the
C
450 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
ECTOPIC BRONCHIAL C O N G E N I TA L A N O M A L I E S
A RT E RY O R I G I N S O F T H E P U L M O N A RY
VESSELS
Undersurface or upper surface of aortic arch
Posterior aortic wall Main Pulmonary Artery
Near left subclavian artery origin
Pulmonary valve stenosis
Lower thoracic aorta
Pulmonary artery stenosis
Brachiocephalic artery
Idiopathic pulmonary artery dilation
Internal thoracic artery
Pulmonary artery aneurysm
Inferior phrenic artery
Persistent truncus arteriosus
Pulmonary atresia
Aorticopulmonary window
Absent pulmonic valve
FIGURE 14-11 Spinal artery branch (arrow) arising from a left Distal Pulmonary Arteries
posterior intercostal artery.
Peripheral pulmonary artery stenosis
B C
FIGURE 14-12 Intralobar pulmonary sequestration. A, A hypervascular multicystic mass in the left lower lobe is identified by computed
tomography. B, Celiac arteriogram shows a massively enlarged left inferior phrenic artery crossing the hemidiaphragm to supply the
sequestration. C, The late-phase arteriogram shows venous drainage into the pulmonary veins.
Imaging
CHEST RADIOGRAPHY
preexisting cardiopulmonary disease. In patients with Chest radiographs are useful for suggesting other diag-
previously normal heart and lungs, small emboli noses (e.g., pneumonia or congestive heart failure) and
produce little effect. However, when the clot burden are critical for interpretation of radionuclide lung scans.
overwhelms the pulmonary circulation reserve, right Many patients have nonspecific abnormalities, such as
ventricular and pulmonary artery pressures rise vague parenchymal densities, areas of atelectasis, or
sharply. This situation may lead to right ventricular pleural effusions. Findings that are more suggestive of
dilation, ventricular failure, and ultimately cardio- PE are rounded or wedge-shaped pleural-based opacities
genic shock. Mortality for patients who present with reflecting pulmonary infarction (Hampton hump), local
some hemodynamic compromise is 20% to 30% and oligemia (Westermark sign), and central pulmonary ar-
approaches 60% in the presence of cardiogenic shock.27 tery enlargement (Fig. 14-13).
Although this bleak picture usually accompanies mas-
sive PE, even small emboli can start such a chain of COMPUTED TOMOGRAPHY ANGIOGRAPHY
events in individuals with underlying heart or lung In most centers, computed tomography (CT) angiogra-
disease. In some patients, inadequate bronchial artery phy is the principal imaging study for the diagnosis of
collateral circulation to the obstructed region results in acute PE.36,37 The sensitivity and specificity with helical
pulmonary infarction. single or 4-detector row scanners is 83% to 100% and
In patients who survive the acute insult, the natural 92% to 100%, respectively38-44 (Figs. 14-14 and 14-15).
history of PE is often endogenous lysis of clot over a Even though the accuracy of commonplace 64-detector
period of weeks.28 About half of patients experience row scanners compared with catheter angiography (the
complete resolution of clot; the remainder have partial gold standard for many decades) has not been rigor-
resolution or chronic obstruction.29,30 Other nonthrom- ously proven, they are considered at least as and prob-
botic causes of PE include septic foci, fat, air, amniotic ably more accurate for diagnosis than older machines.
fluid, intravascular tumor deposits, and medical devices The negative predictive value of CT angiography
(e.g., catheter fragments).31-33 approaches 99%.36,45-48 One prospective study (which
used clinical probability and D-dimer testing along
Clinical Features and Diagnosis with imaging) and a recent metaanalysis of the existing
PE is a grossly underdiagnosed problem. Physicians literature evaluated the negative predictive value of
must remain alert to the possibility in any patient with CT angiography at 3-month follow-up.49,50 The results
cardiopulmonary symptoms or signs and risk factors were remarkably consistent: frequency of missed ve-
for venous thromboembolic disease. The most com- nous thromboembolic events and fatal PE were 1.3% to
mon complaints are chest pain, shortness of breath, 1.4% and 0.5%, respectively. Finally, CT provides a thor-
cough, tachypnea, and tachycardia. With massive PE, ough evaluation of the lungs, heart, and mediastinum,
14. PULMONARY AND BRONCHIAL ARTERIES 453
A B
A B
FIGURE 14-14 A and B, Acute right and left pulmonary artery emboli (arrows) are identified by computed tomography angiography.
HCC, hepatocellular carcinoma; HU, Hounsfield units; RCC, renal cell carcinoma;
RADIONUCLIDE LUNG SCANNING SVC, superior vena cava.
For many years, ventilation-perfusion (V/Q) lung scan-
ning was widely used for evaluating patients with sus-
pected pulmonary embolus. Because it is less specific than system established in the Prospective Investigation of
state-of-the-art CT angiography and a definitive diagnosis Pulmonary Embolism Diagnosis trials (PIOPED-I and -II),
cannot be made in a substantial number of cases, it has which evaluated the diagnostic usefulness of V/Q scan-
assumed a minor role in most centers. Nonetheless, V/Q ning for acute PE.56 Two important conclusions can be
scanning can be useful in some situations:54 drawn from the results of the PIOPED-I studies:
History of anaphylactic reaction to contrast 1. The likelihood of pulmonary embolus in patients
material or severe renal dysfunction with normal scans (4%) and in patients with
Severe tachypnea or combative patient not suitable low-probability scans plus a low clinical index of
for CT angiography suspicion (4%) effectively excludes the diagnosis.
Pregnancy (first or second trimester) 2. The likelihood of pulmonary embolus in patients
Equivocal CT angiography and low clinical with high-probability scans (87%) supports
probability definitive treatment if there is no risk factor
for anticoagulation.
Lung perfusion scans are performed by intravenous
injection of technetium-99m (99mTc)labeled macroag-
gregated albumin particles. Pulmonary emboli produce LOWER EXTREMITY DUPLEX SONOGRAPHY
localized perfusion defects55 (Fig. 14-17). Perfusion Because most pulmonary emboli arise from the legs
defects also may be seen in areas of lung consolidation, and because treatment of PE is aimed at prevention of
lung collapse, and vasoconstriction because of hypoxia recurrent embolism, some practitioners initially per-
(e.g., chronic obstructive pulmonary disease), among form leg duplex sonography to detect potential sources
other reasons. Ventilation scanning is done to exclude of recurrent emboli. Deep vein thrombosis of the leg is
such entities by imaging after the patient inhales 99mTc- detected in patients with suspected PE less than 25% of
diethylenetriamine-pentaacetic acid aerosol. the time.57-59 Likewise, up to 50% of patients with
Several classification schemes have been proposed for proven PE have no sonographic evidence of proximal
interpreting V/Q scans. A widely accepted one is the clot at the time of examination.27 Sonography may be
14. PULMONARY AND BRONCHIAL ARTERIES 455
A B
FIGURE 14-17 Ventilation-perfusion lung scan for pulmonary embolism. A, The perfusion scan in six projections shows large segmental
defects in the right lower lobe. B, The ventilation scan in the posterior projection shows that defects are mismatched.
most useful in individuals with equivocal or low prob- by contrast material (Fig. 14-18). Secondary signs of an
ability V/Q scans when clinical signs of deep venous acute embolus include abrupt vessel cutoff, regional
thrombosis or risk factors for venous thromboembolic hypoperfusion, slow flow, pruning of vessels, and filling
disease are present. of collateral vessels. Emboli are often multiple and bilat-
eral. They tend to lodge in the lower lobes more often
MAGNETIC RESONANCE IMAGING than in the upper lobes.66 Several other disorders can
Promising results have been obtained with MR angiog- cause pulmonary artery obstruction, and some may be
raphy for PE diagnosis. The reported sensitivity and identified at angiography (e.g., chronic thromboembolic
specificity of gadolinium-enhanced MR angiography is disease, tumor, arteritis) 67 (Fig. 14-19 and Box 14-5).
77% to 100% and 95% to 98%, respectively.60-62 However,
multidetector row CT is more accurate than MRI be-
Treatment
cause it has better spatial resolution and produces fewer
artifacts.36 MEDICAL THERAPY
Because many pulmonary emboli undergo spontaneous
CATHETER ANGIOGRAPHY lysis and most patients survive a single episode of PE,
For decades, pulmonary arteriography was considered the primary goal of treatment is prevention of recurrent
the final arbiter in PE diagnosis, but this is no longer PE and progression of thrombosis in the pulmonary
true. Multidetector row CT angiography is probably as arteries. Anticoagulation with intravenous unfraction-
accurate; in fact, even expert angiographers misdiag- ated heparin followed by oral warfarin (Coumadin) for
nosed isolated subsegmental emboli in up to one third of 3 to 6 months was the standard therapy for decades.
cases.63-65 Because it is invasive, expensive, and requires Now, treatment begins with at least 5 days of a low mo-
experienced operators, pulmonary arteriography is now lecular weight heparin (e.g., enoxaparin [Lovenox]) or the
relegated to diagnosis of equivocal cases or planning for pentasaccharide fondaparinux (Arixtra), both given by
endovascular therapy. subcutaneous injection without the need for monitor-
The only reliable angiographic sign of acute PE is an ing68,69 (see Chapter 3). The patient is often switched to
intraluminal filling defect at least partially surrounded Coumadin, which is continued for 3 months or more70
456 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
C D
A B
C
14. PULMONARY AND BRONCHIAL ARTERIES 457
CATHETER ANGIOGRAPHY
BOX 14-6 The technique for bronchial arteriography is outlined
earlier in this chapter. An empirical search is made for
C AU S E S O F M A S S I V E the bronchial arteries on the affected side (see Figs. 14-5
HEMOPTYSIS and 14-10). Bronchial arteries arise from the aorta and
pass to the hila of the lungs, where they become tortuous
Infection and then give off numerous branches. If a bleeding
Tuberculosis source cannot be found, a descending thoracic aortogram
Fungus (e.g., mycetoma) with the catheter placed above the left subclavian artery
Chronic pneumonia to identify bronchial or nonbronchial system collateral
Abscess vessels (especially intercostal or inferior phrenic arteries)
Cystic fibrosis may be helpful99 (Fig. 14-21).
Bronchiectasis or chronic bronchitis The classic findings with bronchial artery bleeding are
Neoplasm enlargement of the main artery (!2 mm), hypervascularity,
Trauma parenchymal stain, and bronchial to pulmonary artery
Iatrogenic (e.g., pulmonary artery balloon shunting (Fig. 14-22). Frank extravasation is uncommon;
catheter) it need not be present to warrant embolization. It is critical
Anticoagulant therapy to look for small branches to the anterior spinal artery,
Pulmonary arteriovenous malformation which usually arise from the proximal portion of the
Vasculitis vessel and take a characteristic hairpin turn as they pass
Pulmonary embolus superiorly and then inferiorly into the anterior spinal
Pulmonary hypertension cord in the midline (see Fig. 14-11).
Mitral stenosis After one or more abnormal bronchial arteries is iden-
Congestive heart failure tified and embolized (see later discussion), potential
Congenital nonbronchial systemic collaterals should be studied
Idiopathic (cryptogenic) (Fig. 14-23 on p. 461). The more common sources are88,99,100:
Internal thoracic (mammary) artery
Thyrocervical branch of the subclavian artery
Lateral branches of the subclavian or axillary artery
upper airway hemorrhage. Localization of the bleeding
Intercostal arteries
site is very helpful before arteriography. Serial changes in
Inferior phrenic artery
chest radiographs or CT scans may suggest the involved
lobes. Fiberoptic bronchoscopy often is used to identify As a rule, collaterals come from vessels in proximity to
the site of bleeding, guide embolotherapy, and, in some the bleeding site (e.g., lower lobe lesions may be fed by an
cases, coagulate the culprit lesion.85 Blood transfusion inferior phrenic artery). Rarely, collateral vessels arising
and correction of coagulation deficiencies should be on the opposite side are responsible for bleeding. If neither
underway at the time of angiography. Airway protection a bronchial nor nonbronchial systemic arterial source
may be necessary if the bleeding is exuberant. Because of can be found, a pulmonary angiogram is performed to
the remote possibility of spinal cord injury from bronchial exclude a pulmonary artery lesion (Fig. 14-24).
artery embolization, a complete neurologic examination
should be documented in the medical record.
Treatment
BRONCHIAL ARTERY EMBOLIZATION
Imaging
PATIENT SELECTION Embolotherapy is the first-line
COMPUTED TOMOGRAPHY treatment for massive hemoptysis or recurrent intractable
In some centers, CT angiography is replacing flexible hemoptysis.101,102 Presence of a major spinal artery or
bronchoscopy in selected individuals with significant radiculomedullary branch from the target artery is
hemoptysis.93 Properly performed CT angiography is considered a contraindication to embolotherapy by some
extremely helpful before bronchial arteriography. It iden- interventionalists, but others perform embolization if a
tifies ectopic bronchial artery origins, depicts nonbronchial microcatheter can be negotiated well beyond such a vessel.
systemic collateral vessels, and detects pulmonary artery
origin for bleeding.94-98 On raw axial images, the bron- TECHNIQUE If the diagnostic catheter (without side
chial arteries appear as clusters of discrete enhancing dots holes) can be advanced deep into the artery, embolo-
near the midthoracic aorta that course in a craniocaudal therapy is performed directly without a significant risk
direction (Fig. 14-20). of refluxing material into the aorta. Usually, however,
14. PULMONARY AND BRONCHIAL ARTERIES 459
A B
C D E
FIGURE 14-20 Bronchial artery embolization for massive hemoptysis from cystic fibrosis. A, Chest radiography shows classic pattern of
widespread cystic bronchiectasis and large bilateral pulmonary arteries. Bronchoscopy identified active bleeding from the right upper lobe
bronchus. B and C, High-resolution chest computed tomography (CT) shows several possible bronchial artery origins (arrowheads) from the
descending thoracic aorta. With guidance from the CT images, the responsible vessel was catheterized quickly. Through the 5 Fr catheter,
a coaxial microcatheter was advanced well into the bronchial artery (D). Note massively enlarged bronchial artery and prominent
hypervascularity. E, Finally, the vessel was embolized with 300- to 500-"m Embospheres to stasis.
a coaxial microcatheter system is negotiated well into A bottle of PVA particles or microspheres is prepared
the bronchial artery beyond intercostal or mediastinal as a slurry made with contrast material (see Video 3-18).
branches (Fig. 14-25 on p. 462). A slow and steady injection is made with continuous
Although a variety of materials has been used for visualization under fluoroscopy until blood flow is
bronchial artery embolization, the most popular agents sluggish. Injection is stopped promptly if reflux along
are polyvinyl alcohol particles (PVA), microspheres the microcatheter is detected. In addition, delayed filling
(e.g., Embospheres), and Gelfoam pledgets103-107 (see of branches to the anterior spinal artery should be con-
Chapter 3). PVA and microspheres usually cause long- tinuously sought. Sometimes, small pledgets of Gelfoam
term occlusion of distal arteries and prevent recruit- are deployed to complete the embolization. Coils should
ment of collateral vessels that may lead to rebleeding. not be used unless they are deposited in side branches
Particle sizes between 250 and 700 "m are used. Smaller before particulate embolization to prevent occlusion
particles could pass through small spinal artery of parietal vessels (e.g., intercostal portion of bronchoin-
branches. Patients with large bronchopulmonary artery tercostal trunk) (see Fig. 14-23).
shunts may require larger sizes to avoid pulmonary in- In almost 5% of cases, the bleeding source is the pul-
farction or systemic embolization through small arterio- monary artery. If CT angiography was not recently done,
venous shunts.108 Gelfoam pledgets also have been used catheter pulmonary arteriography must be performed if
successfully by some practitioners, although this mate- no systemic arterial source is identified. When present, the
rial is resorbed over a period of weeks. usual cause is a peripheral aneurysm or pseudoaneurysm.97
460 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
FIGURE 14-22 Right bronchial arteriogram in a patient with COMPLICATIONS Some patients develop a postembo-
massive hemoptysis from actinomycosis. Characteristic findings include lization syndrome consisting of fever, chest wall pain, and,
bronchial artery enlargement, hypervascularity, and shunting to the rarely, dysphagia. Symptoms may be severe and can last
pulmonary artery branches (arrow). The parenchymal stain is prominent.
for up to 1 week. Complications from embolotherapy occur
in about 2% to 5% of cases and include nontarget emboliza-
tion and bronchial or esophageal necrosis. There is a risk
Embolization of a pulmonary artery aneurysm or pseu- of pulmonary infarction if bronchial embolization is per-
doaneurysm is accomplished using coils to cover the neck formed in the presence of pulmonary artery (or branch)
of the aneurysm109 (see Fig. 14-24). Some of these cases occlusion.112 The most dreaded but extraordinarily rare
also require concomitant embolization of bronchial artery complication is transverse myelitis from inadvertent
branches that may also feed the vascular lesion. embolization of a branch to the anterior spinal artery.113
14. PULMONARY AND BRONCHIAL ARTERIES 461
A B
A B
BOX 14-7
COMMON COMPUTED
TOMOGRAPHY FINDINGS
I N P U L M O N A RY
H Y P E RT E N S I O N
Vasculitis
A wide variety of vasculitides may attack the pulmo-
nary arteries138-140 (Box 14-8). TA is an inflammatory FIGURE 14-28 Takayasu arteritis of the right pulmonary artery.
vasculitis of large- and medium-sized elastic arteries141,142 Notice the long, smooth luminal narrowing and wall thickening.
(see Chapter 1). The classic disease is seen in young
to middle-aged women. Although involvement of the
thoracic and abdominal aorta is almost universal, the individuals with Behet disease (particularly young men)
pulmonary arteries are affected in about 50% of cases.143 develop solitary or multiple hilar or parahilar pulmonary
Pulmonary TA is usually bilateral and most commonly artery aneurysms that are prone to thrombosis or fatal
targets the segmental branches. Imaging shows wall rupture.149-151 Endovascular therapy is undertaken to
thickening and enhancement, luminal stenoses and frank emergently treat or prevent aneurysm rupture.152-155 Pul-
occlusions, or aneurysms and patchy areas of parenchy- monary artery stenoses have also been reported in this
mal low attenuation144 (Fig. 14-28). Both angioplasty and entity (Box 14-9).
stents have been employed in treating symptomatic
patients with chronic pulmonary TA.145
Aneurysms
The collagen-vascular diseases are associated with
a pulmonary vasculitis with fibrotic proliferation in Aneurysms and pseudoaneurysms of the pulmonary
small pulmonary vessels.146 Pulmonary hypertension arteries have many causes156,157 (Box 14-10; see also
may result. Fig. 14-24). Dilation of the main pulmonary artery usually
Behet disease is a multisystem disorder characterized by is seen with left-to-right shunts (Eisenmenger physiology)
aphthous ulcers of the mouth and genital area and ocular or pulmonary artery hypertension. Post-stenotic dilation
involvement147,148 (see Chapter 1). A small percentage of from pulmonary valve or root disease can mimic an
14. PULMONARY AND BRONCHIAL ARTERIES 465
Arteriovenous Malformations
BOX 14-10 (Online Case 48)
C AU S E S O F P U L M O N A R Y Pulmonary AVMs may occur sporadically, but up to
A RT E RY A N E U RY S M S A N D 80% to 90% are found in patients with hereditary hemor-
P S E U D O A N E U RY S M S rhagic telangiectasia (HHT), formerly known as Osler-
Weber-Rendu syndrome.168-170 HHT is an autosomal
Infection (mycotic) dominant genetic disorder marked by telangiectasias
Cavitary tuberculosis (Rasmussen aneurysm) of the mouth and telangiectasias or AVMs of the gastro-
Septic emboli intestinal tract, brain, liver, and lung (see Chapter 1).
Necrotizing pneumonia About 30% to 40% of patients with HHT have pulmo-
Syphilis nary AVMs, and about 60% have multiple lesions.171,72
Trauma Spontaneous epistaxis is the hallmark of the disease.
Pulmonary artery catheterization Family members of affected individuals should be
Pulmonary artery hypertension evaluated, because about one third of them will also
Vasculitis have pulmonary AVMs. Screening is done with con-
Behet disease trast (echo-bubble) echocardiography, arterial blood
Takayasu arteritis gas measurements, and helical CT scanning.92
Connective tissue disorders About 85% of pulmonary AVMs are simple (single
Noninflammatory vasculopathies segmental arterial supply), and 5% to 10% are complex
Marfan syndrome (multiple segmental arterial supply).173-175 They are most
Tumor commonly found in the lower lobes. Diffuse pulmonary
Congenital disorders AVMs and acquired lesions (e.g., in setting of hepatopul-
monary syndrome or trauma) account for the remaining
cases.169,175,176 The AVM causes a right-to-left shunt and
provides an open pathway between the venous and arte-
aneurysm. Central right or left pulmonary artery aneu- rial circulations. Patients may present in early middle age
rysms usually are caused by congenital disorders or with dyspnea, fatigue, hemoptysis, hemothorax, stroke,
vasculitis (e.g., Behet disease). Multiple aneurysms are or brain abscess. However, AVMs often are found inci-
typical with infection (e.g., septic emboli) and arteri- dentally on chest radiographs. The primary rationale for
tis.158,159 Large pulmonary artery aneurysms are often obliterating them is prevention of devastating neurologic
incidental findings on chest radiographs or CT scans; on complications.
occasion, they are detected when hemoptysis, dyspnea, or CT angiography is exquisitely sensitive for detect-
chest pain develops. Some aneurysms can be managed ing lesions that require treatment ($3 mm diameter
successfully with embolization.90 feeding artery) 177 (Fig. 14-29). Pulmonary angiography
466 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
E
FIGURE 14-29 Symptomatic, complex pulmonary arteriovenous malformation in a patient with hereditary hemorrhagic telangiectasia. A, Head
computed tomography (CT) documents old bland stroke with no apparent risk factors. Frontal (B) and lateral (C) chest radiographs show the well-defined
lobular mass at the left lung base (arrowheads). D and E, Chest CT scans confirm the arteriovenous malformations, although the vascular anatomy was
confusing.
14. PULMONARY AND BRONCHIAL ARTERIES 467
is performed for confirmation and embolotherapy, first coil is partially deployed in a small sidebranch
which is the treatment of choice. Pulmonary artery (anchor technique). Alternatively, the first coil is
pressure should be measured; pulmonary hypertension very oversized and composed of stainless steel with
is not uncommon. Selective arteriography in multiple high radial force (scaffold technique). Nester or
projections is necessary to map out the arterial supply. tornado platinum coils are good choices for the
Great care must be taken to avoid allowing room remainder of the vascular occlusion. These long, highly
air into the catheter after it is in a selective position radiopaque coils can be packed densely into the feed-
in the segmental artery feeding the malformation. ing vessel to prevent recanalization.179 Recently, the
Guidewires are always withdrawn from catheters in a Amplatzer vascular occluder has been used in this
saline bath to prevent even minute air bubbles from setting180 (see Chapter 3). While initially effective in
escaping into the systemic circulation. Angiography most cases, late recanalization has been reported.181 In
shows one or more dilated segmental arteries (often the minority of individuals with very high flow or
with several subsegmental branches) feeding an an- dilated arteries, embolization may be done through
eurysmally dilated sac with rapid venous outflow the endhole of an inflated occlusion balloon. Patients
(see Fig. 14-29 and Fig. 14-30). with numerous lesions often require multiple treat-
The technique popularized by White utilizes a long ment sessions.
guiding catheter (7-Fr Lumax device) along with The definition of success is controversial. Some
a 5-Fr diagnostic catheter.172 Patients are fully heparin- experts require near complete fibrosis of the aneurysm
ized and receive antibiotic prophylaxis with cephazo- sac on follow-up non-enhanced CT; others claim par-
lin. Many devices have been used for occlusion, tial success with aneurysm sac size shrinkage to less
including coils and detachable balloons. Coils are than 30% and reduction in feeding artery diameter to
chosen to be at least 1 to 2 mm larger than the artery less than 3 mm.168,169 Success ranges from 75% to 97%.*
being embolized and should be deposited as close as Reasons for delayed failure include recanalization of
possible to the aneurysmal enlargement near the nidus
of the malformation. To ensure a stable coil nest, the *See references 168, 169, 174, 178, 182, 183.
468 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
C D
FIGURE 14-30 A simple pulmonary arteriovenous malformation in a young woman with hereditary hemorrhagic telangiectasia. A, single
enlarged segmental artery feeds the lesion. B and C, Later phases of angiogram show rapid washout into a huge draining pulmonary vein.
D, The lesion is occluded with macrocoils.
14. PULMONARY AND BRONCHIAL ARTERIES 469
embolized vessels, visualization of unrecognized feed- in the field recommends noncontrast chest CT 1 year
ing vessels in complex AVMs, and development of after treatment and every 3 to 5 years thereafter.169,172
bronchial artery collaterals that enter the artery be- Earlier imaging is mandatory if symptoms develop or
yond the embolization site. A postembolization syn- pregnancy is planned.
drome with fever or pleuritic chest pain is common
(about 15% of cases). Serious complications, including
Inflammatory Diseases and Neoplasms
paradoxical embolization of coils or air (which may
produce coronary ischemia, transient ischemic attack, Fibrosing (chronic sclerosing) mediastinitis is a long-
or stroke), occur in less than 5% of procedures. The standing inflammatory process that can present as a
likelihood of major stroke is estimated at 0.5%.184 primary (idiopathic) or secondary disorder (usually
Long-term follow-up CT imaging is important related to previous Histoplasma capsulatum infection).185
to ensure permanent lesion closure. It is also reported The interventionalist might encounter patients with the
that at least 25% of treated patients will demonstrate focal (rather than diffuse) type of the disease, in which
subsequent growth of initially undetectable AVMs or a localized (and sometimes calcified) mass causes ob-
enlargement of the feeding artery to previously small struction of pulmonary vessels, the superior vena cava,
lesions that now warrant treatment.169 A leading expert airways, or the esophagus (Fig. 14-31). Endovascular
A B
D E
C
FIGURE 14-31 Pulmonary artery obstruction from fibrosing mediastinitis. A, Lung perfusion scan shows markedly diminished blood flow
to the right lower lobe. B, Chest computed tomography reveals a calcified extrinsic mass impinging on the descending right pulmonary artery,
a finding that was confirmed on right pulmonary arteriography (arrow) (C). D, Measurements of adjacent normal vessel diameter and stenosis
length are made, and then a balloon expandable stent was inserted. E, Final arteriography shows a widely patent vessel. The patients exercise
tolerance improved markedly soon afterward.
470 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
C
FIGURE 14-32 Pulmonary artery sarcoma. Contrast-enhanced axial (A and B) and coronal reformatted (C) images on computed tomography
show tumor extending throughout the main and right pulmonary artery.
stents are sometimes used to relieve symptoms such as Primary and secondary malignancies of the pulmo-
dyspnea. nary arteries are extremely rare. The most common pri-
Lung neoplasms are associated with vascular encase- mary tumor is pulmonary artery sarcoma, which usually
ment, displacement, or obstruction. Stents and stent- arises in the main, right, or left pulmonary artery and of-
grafts have been used to improve pulmonary artery ten is contained within the lumen186,187 (Fig. 14-32). Dif-
blood flow in selected symptomatic patients with central ferentiation from bland thrombus is occasionally difficult,
obstructions, usually as a palliative measure. Radiofre- although prominent expansion of the vessel suggests tu-
quency ablation has shown promise in treating patients mor rather than bland clot. Transvenous biopsy has been
with unresectable primary and secondary malignancies used to make the diagnosis.152,188 Surgical resection with
of the lung (see Chapter 24). pulmonary artery reconstruction is rarely curative.189,190
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C H A P T E R
15
Lower Extremity Veins
Karim Valji
476
15. LOWER EXTREMITY VEINS 477
A B
478 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
FIGURE 15-3 Normal right lower extremity ascending FIGURE 15-4 Ascending venogram of the left leg shows the
venography. Three paired tibial veins follow the expected course of femoral vein (arrow) and great saphenous vein (arrowhead).
the tibial arteries. They join at the confluence of the superficial inguinal veins
(saphenofemoral junction) in the groin.
Superficial
circumflex Superficial
iliac vein epigastric
vein Giacomini
Superficial vein
femoral vein Superficial
external To deep system
Anterior lateral via perforator
tributary pudendal
vein
Posterior
medial
tributary
Popliteal
Great vein FIGURE 15-5 Superficial venous system
saphenous vein Short of the leg. (Adapted from Min RJ, Khilnani
Anterior saphenous NM, Golia P. Duplex ultrasound evaluation
tributary Posterior vein of lower extremity venous insufficiency. J Vasc
vein arch vein Interv Radiol 2003;14:1233.)
15. LOWER EXTREMITY VEINS 479
the heads of the gastrocnemius muscle bundles and, in veins arise from the upper surface of the common iliac
most cases, joins the popliteal vein around the knee veins. The iliac veins merge at the L4-L5 level to form
at the saphenopopliteal junction. In about one third of the inferior vena cava (IVC).
the population, the SSV communicates with the GSV When a person is supine, a pressure gradient (12 to
directly via the intersaphenous (or Giacomini) vein or 18 mm Hg on the venous side of capillaries; 4 to 7 mm Hg
through another tributary.1 in right atrium) drives blood toward the heart.7 In
Numerous perforating (communicating) veins connect addition, respiratory inspiration accelerates blood
the superficial and deep veins in the calf and thigh. flow centrally. In an upright position, however, lower
The most important of these are the femoral canal per- extremity venous drainage against substantial hydro-
forator (Hunterian, midthigh, and Dodd, lower thigh), dynamic resistance depends on the following: (1) an
paratibial perforator (Boyd, around the knee), and poste- intact muscular pump, (2) competent vein valves, and
rior tibial perforator (Cockett, in the calf). Bicuspid (3) unobstructed outflow. Although the walls of the
valves are situated throughout the deep, perforating, superficial and muscular leg veins contain smooth
and superficial veins of the leg up to the groin. They muscle and are capable of constriction, blood return to
are oriented to direct blood from the superficial to the the heart depends largely on extrinsic compression by
deep system. leg muscles, particularly the calf pump. At rest,
At the inguinal ligament, the common femoral vein blood flows from the superficial system into the deep
becomes the external iliac vein, which is medial to the veins. Competent valves prevent retrograde flow. With
iliac artery (Fig. 15-6). Its tributaries include the pu- muscular contraction, blood is propelled centrally by
bic, deep circumflex iliac, and inferior epigastric veins. forceful emptying of the deep veins.
The external iliac vein courses over the pelvic brim to
the level of the sacroiliac joint, where it joins the inter-
Variant Anatomy
nal iliac vein to form the common iliac vein. The right
common iliac vein is first posterior and then lateral to Duplication of segments of the lower extremity veins is
the iliac artery. The left common iliac vein has a more common. Accessory saphenous veins (which run in the
horizontal course and lies between the right common extrafascial compartment) are described in up to two
iliac artery and the spine. Asymptomatic mild extrin- thirds of the general population.8 Close to one third
sic compression occurs at this site in up to 60% of the of people have duplicated or multiple femoral (or less
general population6 (see Fig. 15-6). Ascending lumbar often, popliteal) veins.9
A B
480 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
Klippel-Trnaunay syndrome (KTS) is a rare congeni- functional disabilities or severe bleeding or cutaneous
tal disorder that features cutaneous capillary malfor- ulcerations.
mations, distorted lower extremity veins (multiple Persistent sciatic vein is a very rare anomaly in which
varicosities and often an ectopic marginal vein), and a remnant of that embryologic vessel remains the pri-
bone and soft tissue enlargement.10-12 A similar but mary venous drainage between the adductor canal and
distinct condition (Parkes-Weber syndrome) includes the internal iliac vein.15,16 The vein is markedly dilated
these elements along with high-flow arteriovenous and tortuous. The disorder may be an isolated condition
malformations. Although most cases of KTS are spo- but often is associated with KTS.
radic and not familial, there is some evidence that the
disease stems from genetic mutations in the angio-
genic protein VG5Q.13
Collateral Circulation
A cutaneous port wine lesion is characteristic. When either the superficial or deep venous system be-
Symptoms include but are not limited to local pain, comes occluded, the complementary network operates
swelling, and bleeding. Sonography and computed as the main collateral pathway. With partial or total iliac
tomography (CT) or magnetic resonance (MR) venog- vein obstruction, transpelvic and ascending lumbar
raphy are useful in mapping the bizarre, disordered veins serve as the chief collateral channels (Fig. 15-8).
venous channels14 (Fig. 15-7). When present, the mar-
ginal vein runs along the lateral aspect of the thigh
and drains into the internal iliac or femoral vein. Mild MAJOR DISORDERS
cases of KTS are managed with compressive stocking
therapy alone. Sclerotherapy and embolotherapy are Acute Deep Venous Thrombosis
used to treat the abnormal venous channels and arte- (Online Case 85)
riovenous malformations associated with this syn-
drome.10 Surgery is reserved for those patients with Etiology and Natural History
Acute lower extremity and pelvic deep venous thrombosis
(DVT) is part of the spectrum of venous thromboem-
bolic disease (VTE, see also Chapter 1). This disorder
also includes pulmonary embolism (PE) and chronic ve-
nous insufficiency (CVI, sometimes called post-thrombotic
or postphlebitic syndrome).17,18 Acute DVT is a common
FIGURE 15-7 Klippel-Trnaunay syndrome. Bizarre, dilated FIGURE 15-8 Chronic left iliac vein occlusion with injection
venous collaterals fill on an ascending venogram in place of a normal from the left common femoral vein. Transpelvic and circumflex iliac
deep venous system. venous collaterals drain the leg.
15. LOWER EXTREMITY VEINS 481
clinical problem, with an overall lifetime risk of about Relative hypercoagulability is the leading culprit in
2% to 5% of the general population.19 most instances.
In humans, thrombi are constantly forming in the Iliac vein thrombosis can occur with propagation of
valve sinuses and venous confluences of the muscular femoropopliteal vein clot. Isolated iliofemoral venous
calf veins. The endogenous fibrinolytic system usually thrombosis (encompassing the common femoral and iliac
dissolves these small clots. Thrombus remains confined veins) accounts for no more than 20% of cases of lower
to the calf veins in about 75% of untreated patients.20 extremity DVT and usually can be attributed to local
The risk of symptomatic PE in this situation is low.21 factors23 (Fig. 15-9 and Box 15-2). Left iliac vein compres-
In the remaining cases, thrombus extends to the proxi- sion (May-Thurner syndrome) frequently is responsible
mal (femoropopliteal) veins. Most of these individuals for left-sided iliofemoral thrombus formation (see later
have more than one predisposing factor to clot for- discussion). Iliofemoral DVT is also remarkable for the
mation, such as sluggish blood flow, vessel injury, or a rarity of complete recanalization, relative resistance
thrombophilic state (i.e., Virchow triad) 7,22 (Box 15-1). to conventional anticoagulative measures, and more
profound (and perhaps frequent) symptoms of post-
thrombotic syndrome (PTS).24
In a small subset of patients, extensive peripheral and
BOX 15-1 iliofemoral thrombosis occurs, leading to an edematous,
painful white leg (phlegmasia alba dolens). If obstruction
R I S K FA C T O R S of collateral channels ensues, venous drainage is almost
FOR VENOUS completely blocked and the patient will suffer from a
THROMBOEMBOLIC markedly swollen, painful cyanotic extremity, some-
DISEASE times with diminished arterial pulses (phlegmasia cerulea
dolens).25 This grave condition (which requires immedi-
Primary and secondary thrombophilic states
ate intervention) may lead to venous gangrene, massive
(see Boxes 1-4 and 1-5)
PE, or death.
Prior history of venous thromboembolic disease
Once acute DVT occurs, the fate of the thrombus is
Immobilization or bed rest
variable7,26 (Box 15-3). The likelihood of a particular out-
Major trauma or surgery
come depends on many factors, but some important
Spinal cord injury
generalizations can be made:
Cancer (and chemotherapy)
Advanced age
The risk for PE is quite low with isolated calf
Central venous catheter
DVT. The risk for symptomatic PE is reduced
Obesity
substantially in patients with proximal DVT
Use of oral contraceptives or estrogen therapy
who are given therapeutic anticoagulation
Pregnancy and puerperium
(from at least 30% to less than 5%).22,27,28
Congestive heart failure
Recurrent DVT is observed in 25% to 50% of
individuals despite adequate treatment.7,29,30
A B
FIGURE 15-9 Right iliofemoral deep venous thrombosis (arrow) caused by posttraumatic right thigh and groin hematoma. Contrast-
enhanced computed tomography scans through the upper pelvis (A) and inguinal region (B). The more peripheral veins were normal.
482 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
Complete clot resolution with unscarred veins foramen ovale or pulmonary arteriovenous malforma-
is much more common in calf and femoropopli- tion). Arterial embolization is the consequence.
teal DVT than often believed. However, recanali-
zation of iliofemoral DVT is uncommon (!30% Clinical Features
of cases).31-33 Patients may complain of acute onset of leg pain, swelling,
Chronic venous insufficiency and PTS or tenderness. Less common signs include distention
(see later discussion) may result from valve of superficial veins, cyanosis, erythema, palpable calf
disruption (with associated reflux) or persistent cords, or Homans sign (calf pain with forced dorsiflexion
venous occlusion. of the foot). However, the symptoms and signs of lower
extremity deep vein thrombosis are notoriously unreli-
Perhaps the most surprising rare sequela of acute
able. Many patients (particularly in the postoperative
DVT is paradoxical embolism with thrombus passing
setting) with proven DVT are asymptomatic, and many
through a right-to-left circulatory shunt (e.g., large patent
others with classic features do not have the disease. PE can
be the first signal of acute DVT. When isolated iliofemoral
DVT occurs, symptoms initially may be confined to the
pelvis and thigh. Iliofemoral DVT occurs more frequently
BOX 15-2 in the left leg than the right and more frequently in women
than men.
C AU S E S O F I S O L A T E D
ILIOFEMORAL VENOUS Diagnosis
THROMBOSIS Although individual clinical signs often are misleading,
predictive rules such as those devised by Wells and
Iliac vein compression (May-Thurner) syndrome colleagues have proven valuable in assessing risk for the
Prior iliocaval deep venous thrombosis disease (Box 15-4). Because the consequences of a missed
Malignancy (benign or malignant) diagnosis and no treatment can be life-threatening,
Pregnancy screening of high-risk asymptomatic patients and accu-
Surgery rate diagnosis of symptomatic patients is critical and
Inferior vena cava filter must depend on risk factor analysis, objective diagnostic
Indwelling catheter tests, and imaging studies, alone or in combination.
Primary thrombophilic state
Trauma
Accidental
Iatrogenic (e.g., prior catheterization)
Benign extrinsic compression (e.g., aneurysm)
Retroperitoneal fibrosis BOX 15-4
Radiation therapy
CLINICAL PREDICTORS
OF ACUTE DEEP VENOUS
THROMBOSIS
Active malignancy
Paralysis, paresis, or recent lower extremity
BOX 15-3
immobilization
F AT E O F A C U T E L O W E R Bedridden for more than 3 days
EXTREMITY DEEP VENOUS Major surgery within 12 weeks
THROMBOSIS Previous deep venous thrombosis
Localized tenderness
Pulmonary embolism Complete leg swelling
Complete clot resolution Calf swelling 3 cm greater than asymptomatic leg
Incomplete recanalization with vein scarring, Unilateral pitting edema
valve injury, and venous reflux Collateral superficial veins (nonvaricose)
Thrombus propagation
Data from Wells PS, Anderson DR, Rodger M, et al. Evaluation
Recurrent deep venous thrombosis of D-dimer in the diagnosis of suspected deep-vein thrombosis.
Persistent occlusion N Engl J Med 2003;349:1227.
15. LOWER EXTREMITY VEINS 483
D-dimer is a byproduct of endogenous fibrin degra- predictive value of a normal compression sonogram at
dation, and plasma levels are elevated in patients with greater than 99.5%.41,42
venous thrombosis or PE. The D-dimer radioimmuno- In asymptomatic patients with risk factors for DVT,
assay has been useful in excluding acute DVT, particu- color Doppler sonography is not as accurate (sensitivity
larly when applied along with predictive rules.19,34,35 47% to 62%).38,43 This discrepancy largely is related to
For example, a negative result from a high-sensitivity the nature of occlusions in this population (i.e., often
D-dimer test (e.g., serum level !500 ng/mL) and a low confined to calf veins, composed of smaller, nonocclu-
Wells score puts the likelihood of acute DVT diagnosis sive, segmental thrombi).
within 3 months at about 0.5%.36 Misdiagnosis is usually related to underlying chronic
venous disease, isolated clot (iliac vein, calf veins, deep
femoral vein, or one limb of a duplicated femoral or
Imaging
popliteal vein) and technical errors. Acute and chronic
SONOGRAPHY DVT can be confused at sonography. Certain features are
Because duplex sonography is extremely accurate, easy to used to differentiate between these entities (Table 15-2).
perform, relatively inexpensive, and completely safe, it is Sometimes, however, it is impossible to distinguish
the principal imaging study in both symptomatic and among an acute clot occupying a previously normal vein,
asymptomatic groups.37-40 Several factors are evaluated a chronic organized clot, and acute clot superimposed on
(Fig. 15-10 and Table 15-1). Sonography also detects other chronic disease (Fig. 15-11). It is for this reason that some
causes for leg symptoms, such as a Baker cyst, lymphade- experts recommend a follow-up sonogram as a baseline
nopathy, hematoma, or popliteal artery aneurysm. study for all patients with acute DVT in the event that
In symptomatic patients, compression and color Doppler symptoms recur.
sonography are about as accurate as traditional contrast The clinical significance of isolated calf vein DVT is
venography in the diagnosis of acute proximal DVT, controversial.28,44,45 Compression sonography and color
with a sensitivity of 89% to 96% and specificity of 94% to Doppler flow imaging are fairly accurate in detecting
99%.37-40 Outcome analyses from two large cohorts of calf vein clot.46,47 In some series, the sensitivity of color
patients with suspected DVT estimated the negative Doppler sonography is comparable in the calf veins and
TABLE 15-2 Sonographic Distinction Between Acute are luminal filling defects, vein wall enhancement, and
and Chronic Deep Venous Thrombosis filling of collateral veins (see Fig. 15-9). Incomplete
Feature Acute DVT Chronic DVT
opacification of vein segments and beam-hardening
artifacts can mimic clot.
Lumen Dilated Narrowed or normal caliber
Luminal flow Absent or minimal Residual flow, reflux MAGNETIC RESONANCE IMAGING
Vein wall Thin Thickened
Collaterals Poorly developed Well developed The accuracy of MR venography in the diagnosis of
Compression Spongy Firm resistance DVT in the leg is similar to contrast venography and
duplex sonography.54-56 However, an MR examination is
DVT, deep venous thrombosis.
more costly and time consuming than a sonogram. Still,
MR imaging (MRI) is superior to sonography for pelvic
proximal veins. But in routine practice, technically inad- vein and IVC disease.
equate studies of the calf are relatively common.40,48
Some practitioners opt for serial examinations of the ASCENDING VENOGRAPHY
proximal veins to identify propagation into the femoro- Although catheter-based contrast venography was once
popliteal system. considered the gold standard in the diagnosis of acute
and chronic DVT, in fact it was not always reliable.57 One
COMPUTED TOMOGRAPHY IMAGING autopsy study revealed a sensitivity and specificity of
Even though CT venography of the lower extremities 89% and 97%, respectively.58 Interobserver variability is
is relatively accurate, it is rarely employed as the initial at least 10% to 15%.59 The procedure is uncomfortable for
step in routine cases. Some centers favor combined CT the patient, and it has a small risk of significant complica-
venography and CT pulmonary angiography in pa- tions. For these reasons, it rarely is used for diagnosis
tients with suspected venous thromboembolic disease.49 anymore.
CT venography is more accurate than sonography in A fresh clot produces an intraluminal, wormlike fill-
the pelvic veins and IVC and may identify the mecha- ing defect (Fig. 15-12). Abrupt occlusion of a vein can
nism for isolated iliofemoral DVT.50-53 Typical findings reflect acute or chronic thrombosis (see Fig. 15-8).
Nonfilling of deep veins, preferential filling of superfi- Treatment of isolated calf vein DVT is controversial,
cial veins, and opacification of collateral veins may because without anticoagulation there is a 20% to 30%
occur with acute or chronic DVT. Thrombus may be risk for clot propagation, a small risk for significant PE,
confused with other causes for nonfilling of portions and about a 30% risk for CVI.31,62,65,69,71 Even without
of the deep venous system. compelling data, many physicians still treat such indi-
viduals with a short course of anticoagulation because
Imaging Strategy they are concerned about proximal extension. Those not
Every physician must develop his or her own algo- treated may undergo follow-up Doppler sonography to
rithm for assessing symptomatic and high-risk pa- exclude clot propagation.
tients for acute DVT using a combination of risk-factor
analysis, lab testing (D-dimer), color Doppler sonog- IVC FILTER PLACEMENT
raphy, and other imaging studies. Periodic surveil- If there is a contraindication to or history of complication
lance of at-risk populations has uncovered lower from anticoagulation, a retrievable IVC filter should be
extremity DVT in up to 28% of patients, about 80% of placed instead (see Chapter 16). The detection of free-
whom were asymptomatic.60-62 Many clinicians order floating iliofemoral or IVC thrombus deserves special
follow-up exams after a normal ultrasound in all cases mention. Even with therapeutic anticoagulation, the pos-
or at least in those with moderate to high clinical sibility of PE exceeds 30%; thus insertion of a retrievable
probability of disease. However, only 1% to 2% of pa- IVC filter is prudent.72
tients with initially negative studies subsequently
are shown to have developed proximal DVT.63,64 CATHETER-DIRECTED ILIOFEMORAL VENOUS
D-dimer results may be used to withhold ultrasound THROMBOLYSIS
in patients with low clinical probability.37 A follow-up There is ample evidence that following an episode of
study after completion of anticoagulant therapy may lower extremity DVT, return of normal valve activity
be advantageous in higher-risk patients should symp- largely is a function of the time to thrombus resolu-
toms recur in order to distinguish chronic disease tion.7,73-75 Thus the main reason for aggressive endovas-
from recurrent acute DVT. cular clot removal in patients with proximal acute DVT
is the prevention of CVI and recurrent DVT. A secondary
Treatment benefit is more rapid symptom relief.
Patients with acute DVT are treated to prevent or limit Systemic thrombolytic infusion is moderately suc-
the major sequelae of venous thrombosis: PE, CVI, and cessful in this situation, but bleeding complications are
recurrent DVT.28,65,66 frequent.76-78 Catheter-directed thrombolysis (with or
without adjunctive mechanical thrombectomy) offers
MEDICAL THERAPY faster, safer, and more effective treatment for acute
The cornerstone of treatment is anticoagulation. In addi- venous thrombosis.79,80
tion, class II (30 mm Hg) elastic compression stockings
are strongly recommended to lessen the risk for PTS.67 PATIENT SELECTION Careful case screening is im-
Anticoagulation does not directly promote fibrinolysis, portant to avoid subjecting unsuitable patients to this
but it allows endogenous lysis to occur and reduces the intensive procedure66,76 (Box 15-5).
likelihood of PE by limiting clot propagation. For many
decades, treatment for DVT consisted of unfractionated The risk for PTS is relatively low in individuals
intravenous heparin (3 to 5 days) and oral warfarin (at with isolated calf DVT or asymptomatic DVT; in
least 3 to 6 months).28,68 In most centers, low molecular those patients, thrombolysis is not warranted.81
weight heparin (e.g., enoxaparin, tinzaparin) or a spe- Patients with subacute or chronic venous thrombosis
cific factor Xa inhibitor (e.g., fondaparinux) has replaced ("2 to 4 weeks), prior ipsilateral proximal DVT,
initial heparin therapy. Low molecular weight heparins nonambulatory state, or short life expectancy
have a more predictable response and a longer duration generally do not benefit from thrombolysis.66,67,79
of action, and they can be given at home once or twice Individuals with subacute or chronic ilofemoral
daily as a subcutaneous injection66,68 (see Chapters 2 and vein occlusion may benefit from angioplasty
3). Monitoring of drug effect is unnecessary except in and stent placement (Fig. 15-13).
certain situations (e.g., obesity, pregnancy, heart or liver Individuals with risk factors associated with
failure). Therapeutic anticoagulation substantially re- fibrinolytic agents or full-dose anticoagulants
duces the likelihood of PE. Even with full compliance, (see Box 3-7) may be suitable for mechanical
however, recurrent DVT still occurs in more than 25% of thrombectomy alone.
cases, and at least one fourth will ultimately suffer from Phlegmasia cerulea dolens is a medical emergency
chronic PTS.31,65,69,70 and demands rapid, aggressive treatment.25,82
486 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
C
15. LOWER EXTREMITY VEINS 487
A B C
D E
FIGURE 15-14 Iliofemoral deep venous thrombolysis. A, Acute thrombus in the left common femoral vein. Disease extends up the iliac
vein and down to the popliteal vein. B, After 18 hours of tissue plasminogen activator infusion from catheters placed from the popliteal and
right internal jugular vein, there is moderate clot dissolution. C and D, After 36 hours of treatment, there is near complete lysis of the entire
diseased segment. E, A Wallstent is placed to treat extrinsic disease in the left common iliac vein, with excellent results.
tissue plasminogen activator (or other alone is not effective in most hands; infusion of a fibrino-
fibrinolytic agent) at about 1 mg/hr lytic drug is mandatory, alone or combined with me-
Ultrasound-assisted thrombolysis with the chanical clot dissolution. Thrombectomy devices may be
EKOS catheter used initially to reduce the clot burden or employed after
Isolated thrombolysis with Trellis infusion system lytic infusion to eliminate residual clots.
Enzymatic lysis combined with Arrow-Trerotola After the bulk of the clot has been removed, bal-
or AngioJet mechanical thrombectomy83-85 loon angioplasty and self-expanding stent placement
(as needed in the iliac and sometimes femoral veins) are
Anticoagulation with heparin is initiated to maintain performed to treat residual disease. Because of the
the partial thromboplastin time (PTT) in the 60- to availability of large diameter stents and resistance to
80-second range. Thrombolysis alone often requires large plastic deformity from extrinsic compression, the Wall-
doses of a fibrinolytic agent and 2 to 3 days of infu- stent is still the favored device (Fig. 15-15; see Fig. 15-14).
sion.79,86-94 Unfortunately, rapid mechanical thrombectomy Following the procedure, patients are maintained on
488 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
C D
FIGURE 15-15 Collapsed iliac vein stent. Axial (A) and magnified (B) computed tomography (CT) scans of a previously placed left iliac
vein balloon expandable stent shows a crushed device (arrow). C and D, Left iliac venography demonstrates an the extensive collateral
circulation that indicates some degree of obstruction.
aggressive anticoagulation for 6 months to 3 years (or catheter-directed thrombolysis for reducing PTS after
indefinitely if a thrombophilic disorder is identified).7 a first episode of acute iliofemoral DVT. The ongoing
Compressive elastic stockings are also strongly recom- CaVenT randomized trial is most compelling in this
mended for 2 years afterward. regard.67 Preliminary findings in the lytic arm in-
cluded 90% moderate to complete lysis, 2% incidence
RESULTS Technical success (using urokinase or tis- of major bleeding complications, reduction of venous
sue plasminogen activator) is achieved in 80% to 95% obstruction at 6 months from 49% to 20%, but no sig-
of cases when the thrombotic disease is acute.* Pri- nificant difference in incidence of femoral venous
mary patency at 1 year ranges from 63% to 90% for the insufficiency (60%).
iliac segment and 40% to 47% for the femoral segment.
There is now very strong evidence for the value of COMPLICATIONS Major bleeding complications
occurred in 11% of cases in the publication from a mul-
tiinstitution venous registry.79 PE attributed to the
thrombolytic procedure itself is reported in about 1%
*See references 80, 84, 88, 89, 95-104. of cases.
15. LOWER EXTREMITY VEINS 489
F
E
FIGURE 15-15, contd E, Following additional stent deployment, venography shows excellent flow. F, Duplex sonography about
6 months later confirms continued patency.
Imaging
Imaging is important in the management of patients
with suspected chronic lower extremity venous dis-
ease. The most important questions to address are pa-
tency of the deep venous system, valvular incompe-
tence in superficial, deep, and perforating veins, the
extent of reflux, and the exact sites of incompetent
veins.
SONOGRAPHY
Color Doppler sonography is the standard test for study-
ing patients with CVI when invasive therapy is being
considered3,112,113 (see Fig. 15-2). With the aid of provoca-
tive measures (e.g., compression of calf veins, Valsalva
maneuver), venous reflux, valvular dysfunction, and
incompetent perforating veins are detected and mapped.
Sonography also identifies persistently occluded or par-
tially recanalized deep veins.
PLETHYSMOGRAPHY
Sonography is an outstanding tool for providing a nar-
row window on focal venous disease of the leg, but it is
relatively useless in assessing the overall dysfunction
of the venous circulation. For that, air or strain-
gauge plethysmography is needed. Both tests measure
changes in limb volume as a reflection of overall venous
A B
hemodynamics.114
FIGURE 15-16 Chronic lower extremity deep venous thrombosis.
COMPUTED TOMOGRAPHY AND MAGNETIC A, Deep veins of the calf remain completely occluded, and venous
RESONANCE IMAGING drainage is entirely through superficial channels. B, Recanalization
of a previously occluded left femoral vein. The vein is irregular,
CT or MR venography can be useful adjuncts to duplex contains several webs (straight arrow), is devoid of normal-
sonography, particularly in the evaluation of chronic appearing valves, and communicates with the deep femoral
pelvic venous disease. vein (curved arrow).
15. LOWER EXTREMITY VEINS 491
A B
FIGURE 15-17 Patient with symptoms of chronic venous insufficiency. A, Pelvic venogram shows recanalized left external and common
iliac veins and lower inferior vena cava with luminal irregularity. Ascending lumbar venous collaterals also are present (arrow). B, After angio-
plasty with a 10-mm balloon and placement of a 14-mm diameter Wallstent, the vein is widely patent.
TABLE 15-3 Revised CEAP Classification System for Chronic MEDICAL THERAPY
Venous Disease The mainstay of therapy for CVI is leg elevation, exer-
Class Stage cise, weight reduction, and graded elastic compressive
stockings (pressure "20 mm Hg).33 Simple, semiocclu-
0 No signs of venous disease
sive, or biologic dressings are applied to the ulcers
1 Telangiectasias, reticular veins
2 Varicose veins themselves.
3 Lower extremity edema without skin changes
4 Skin pigmentation, lipodermatosclerosis ENDOVASCULAR THERAPY
5 Skin changes with healed ulcer Patients with CVI primarily because of venous outflow
6 Skin changes with active ulcer
obstruction may benefit from endovascular treatment,
particularly when disease is confined to the iliocaval
segment.107,116 Fibrinolysis and mechanical thrombec-
tomy devices generally have no role in this situation.
Endovascular recanalization of chronic femoropopliteal
TABLE 15-4 Venous Clinical Severity Score (VCSS)
for Chronic Venous Disease disease is frequently not durable.
After gaining vascular access (to the ipsilateral pop-
Attribute Mild Severe liteal or femoral vein) with sonographic guidance, the
Pain Occasional Limits activities obstruction is crossed with a guidewire and catheter
Varicose veins Few, scattered Extensive (see Fig. 15-17). If the guidewire will traverse the en-
Venous edema Evening, ankle only All day, most of leg tire obstruction but a catheter will not follow, the wire
Pigmentation Limited area Wide area may be snared from an access site on the other side of
Inflammation Cellulitis Severe cellulitis
Induration Focal (!5 cm) Entire lower third
the blocked segment. Tension on the wire from both
of lower leg ends usually permits a catheter to be advanced. Al-
Number of ulcers 1 3 though the wire may be partially in a subintimal loca-
Ulcer duration !3 months "1 year tion, recanalization is still safe. Full anticoagulation is
Ulcer diameter !2 cm "6 cm instituted. Large overlapping stents (e.g., Wallstents)
Compression Rx Intermittent Constant
are laid along the entire occlusion. Typical nominal
For each attribute, score 0 # none, mild # 1, moderate # 2, severe # 3. stent diameters are common femoral/external iliac
492 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
vein 12 mm, common iliac vein 14 to 16 mm, and IVC allow superficial venous reflux.124 In a minority of
16 to 20 mm or more. Ambulation is ordered starting cases, obstruction and valve incompetence in the deep
the next day. Compression stockings are mandatory veins are culpable.111 Primary superficial venous in-
because worsening of venous reflux is the norm. If competence can progress to chronic venous insuffi-
safe, patients receive clopidogrel for 1 to 3 months, fol- ciency with associated skin changes, although many of
lowed by lifelong aspirin, and at least 3 to 6 months of those patients also have chronic deep vein disease (see
warfarin anticoagulation. earlier discussion).
In recent reviews of published experience with this Lower extremity venous insufficiency manifested
disorder, technical success exceeded 90%, midterm as- by telangiectasias and varicose veins afflicts 10% to
sisted patency exceeded 80%, and complete symptom 20% of men and 25% to 33% of women in Western
relief and ulcer healing was observed in about half of populations.1,122 Varicose veins are more common in
cases117-119 In one large series by a leading investigator some families, in obese individuals, in women, and
in the field, not only did clinical symptoms (particularly with advancing age.125
venous claudication) abate in the majority of treated
individuals, but objective improvement in venous flow Clinical Features
and calf pump function also was the rule.117 Not sur- The obvious visual signs of the primary venous insuf-
prisingly, venous reflux worsened, highlighting the ficiency are small telangiectasias and reticular varicosi-
need for compressive stockings. Notably, about one ties (CEAP class 1 disease) and later large varicose
fourth of patients complained of transient back pain veins (class 2 disease). Patients also may complain of
afterward. leg aching, pain, or heaviness, and eventually pos-
tural swelling confined to the foot and ankle (class 3
SURGICAL THERAPY disease). Symptoms are worse with prolonged stand-
The nihilistic view of surgery for chronic venous in- ing and at the beginning of the menstrual period. In a
sufficiency was challenged in a recent trial that minority of cases, pruritic chronic skin changes de-
showed real reduction in venous ulcer recurrence velop (pigmentation or lipodermatosclerosis, class 4
(though not time to healing) after superficial vein disease) followed rarely by venous ulcers (class 5 or 6
surgery plus compressive therapy compared with disease).
compressive therapy alone.120 However, the role of
surgical repair for deep and perforating vein incompe- Imaging
tence is controversial. Options include vein transfer, Ultrasound is the primary modality for assessing
internal valvuloplasty, subfascial endoscopic perfora- patients with superficial venous incompetence and
tor surgery (SEPS), and extrafascial perforator liga- associated symptoms.1,2,124,126,127 Marked enlargement
tions. When endovascular methods fail, iliac vein of the GSV ("4 mm) or SSV ("3 mm) is evident. At
obstruction can be managed with a femorofemoral the level of major valves, prolonged reversal of flow
vein crossover graft using saphenous vein (Palma ("0.5 sec) is observed with Doppler waveform analy-
procedure).121 Sometimes, the surgeon will construct sis after manual compression of upstream venous
a temporary distal arteriovenous fistula to improve beds (see Fig. 15-2). Reflux in the main channels
patency. is traced to the level of incompetent tributaries
and superficial varicosities. In particular, the antero-
Varicose Veins and Primary Venous lateral and posteromedial channels should be as-
Insufficiency sessed. Even following saphenous vein ligation, the
sonographer may identify persistent refluxing seg-
Etiology and Natural History ments of the GSV or enlarged major tributaries.
(Video 15-1 and Online Case 98) The most common patterns are insufficiency at the
Primary venous insufficiency must be distinguished from confluence of the superficial inguinal veins, allowing
the secondary form discussed earlier.122 The precise GSV reflux, insufficiency of the femoral canal
etiology is obscure, but prevailing research points to perforator with lower GSV reflux, external pudendal
underlying structural defects in the vein wall that are vein reflux leading to GSV reflux, and incompetence
ultimately responsible for valve failure and vein en- of the intersaphenous vein leading to GSV and
largement.123 Regardless of the reason for valve dys- SSV reflux. Again, after clinical evaluation and ve-
function, both hydrostatic forces (column of blood act- nous imaging, the extent of disease is classified ac-
ing unopposed on superficial veins) and hydrodynamic cording to the CEAP scheme to optimize communica-
ones (calf muscle pump acting on subcutaneous veins tion among providers and guide treatment115 (see
in the absence of functional perforating valves) work to Table 15-3).
15. LOWER EXTREMITY VEINS 493
A B
C
15. LOWER EXTREMITY VEINS 495
jugular route avoids damage and possible thrombosis of (Fig. 15-19). However, occult venous damage is rela-
the inflow vein, which could jeopardize the results of the tively common and ultimately can lead to DVT or PE.
procedure. Patients are heparinized during the interven- Color Doppler sonography is an excellent tool for
tion. Self-expanding stents (e.g., Wallstents) generally are screening the leg in this population; its accuracy is
preferred because many of these lesions have a compo- similar to that of contrast venography.149 Unsuspected
nent of extrinsic compression that could cause perma- venous trauma may be discovered at the time of sur-
nent plastic deformation and crushing of a balloon- gery for an associated arterial injury. The vein is
expandable device (see Fig. 15-15). Typically, a 14- to treated by direct repair, bypass grafting, or ligation.7,150
16-mm diameter stent is necessary in the common and As a life-saving measure, an occlusion balloon may
external iliac veins. be inflated to halt exsanguinating hemorrhage and
Some experts favor anticoagulation with warfarin after allow definitive repair.151
stent placement. Recanalization is successful in greater
than 90% of cases.141,144,145 The 1-year primary patency rate
Aneurysms
ranges from about 50% to 80%. Malignant obstructions are
more prone to late occlusion than are benign strictures. Aneurysms of pelvic and extremity veins are exceed-
Major complications are reported in up to 7% of cases ingly rare152,153 (Fig. 15-20). By far, the most common site
and include access site bleeding, stent malposition, and is the popliteal vein. The diagnosis usually is made
stent migration. Traditional concerns about placing self- by color Doppler sonography. Because of the likelihood
expanding stents across the hip joint may be unfounded.146 for clot formation and subsequent PE, venous recon-
struction often is performed.
Trauma
Venous Malformations
Lower extremity venous trauma requires specific ther-
apy far less often than does arterial trauma, and imag- Congenital venous malformations of the legs are consid-
ing is rarely needed to evaluate potential injuries147,148 ered in Chapter 8.
B
FIGURE 15-19 Iliac vein injury from blunt trauma. A and B, Contrast-enhanced computed tomography images show abnormal dilation
of the left iliac vein (arrow) with surrounding density representing blood.
496 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
B C
FIGURE 15-20 Iliac vein aneurysm. An incidentally detected massive left external iliac vein aneurysm is noted on a longitudinal
ultrasound (A) and later on preoperative catheter venography (B). The right common and external iliac veins are also dilated (C).
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C H A P T E R
16
Inferior Vena Cava
Karim Valji
INFERIOR VENACAVOGRAPHY
Normal Anatomy (Online Case 11)
Inferior venacavography is performed through the right The IVC begins at the confluence of the common iliac
internal jugular (IJ) vein or either common femoral vein veins, which corresponds to the L4-L5 level2,4 (see Fig. 16-1
(CFV). The jugular route must be taken in patients with and Fig. 16-2). The left common iliac vein and iliocaval
bilateral common femoral, iliac vein, or inferior vena junction pass between the right common iliac artery and
cava (IVC) thrombosis. Real-time sonographic guidance the spine at this site. The IVC ascends in the retroperito-
is mandatory for IJ vein puncture and is helpful for neum to the right of the aorta. In the midabdomen, the
access at the groin. In some patients, the CFV lies pos- IVC courses behind the head of the pancreas, the superior
terior or posteromedial to the common femoral artery. portion of the duodenum, and the portal vein. The vessel
To avoid traversing the artery, a single-wall needle is then runs in a groove on the posterior surface of the liver.
slowly inserted through the skin toward the vein with As it traverses the diaphragm, it is enveloped by the
continuous aspiration on the needle hub. pericardium and then enters the inferoposterior aspect
Number 4- or 5-French (Fr) pigtail (or similarly shaped) of the right atrium (RA). The eustachian valve is located
catheters are used for venacavography with the side holes on the right lateral side of the IVC at its junction with
placed at the common iliac vein confluence. Sizing cath- the RA. Otherwise, the IVC has no valves. The ascending
eters with radiopaque markers assist in determining caval lumbar veins originate from the common iliac veins and
diameter in patients undergoing IVC filter placement. run alongside the vertebral bodies (Fig. 16-3). Above
When iodinated contrast must be avoided because of re- the L2 level, they drain into the azygous system (see
nal insufficiency or history of severe contrast allergy, CO2 later discussion). Four pairs of lumbar veins connect
is used.1 A typical injection rate with iodinated material is the IVC with the bilateral ascending lumbar channels
15 mL/sec for 2 seconds. With CO2 venography, rapid (Fig. 16-4).
manual injection of 40 to 60 mL is necessary for adequate The renal veins empty into the IVC about the L1-L2 level
opacification. CO2 venography is prohibited in patients (see Figs. 16-2 and 16-4). Renal vein anomalies (e.g., mul-
with a documented right-to-left circulatory shunt. tiple veins, circumaortic or retroaortic left renal vein) are
seen in up to 30% of individuals5 (Fig. 16-5; see also Figs.
10-8 and 10-9). The right gonadal vein enters the IVC just
ANATOMY below the right renal vein, and the left gonadal vein enters
the undersurface of the left renal vein lateral to the verte-
bral column (see Fig. 16-4). The right adrenal vein drains
Development into the right posterior wall of the suprarenal IVC in a
The posterior cardinal veins drain the caudal aspect of horizontal plane at about the T12 level (see Figs. 13-8 and
the fetus during the first weeks of development.2,3 By the 13-9). In contradistinction, the left adrenal vein joins the left
seventh week of gestation, these vessels start to involute, renal vein in a vertical plane as a common trunk with the
and the subcardinal and supracardinal venous channels left inferior phrenic vein (see Fig. 16-4; see also Fig. 10-3).
emerge (Fig. 16-1). In the middle of the abdomen, the The right, middle, and left hepatic veins converge at the
paired systems fuse into a vascular sinus, the subcardinal- upper IVC just below the diaphragm (see Fig. 12-4). In
supracardinal anastomosis. The normally positioned right- many individuals, more caudally positioned accessory
sided IVC and the azygous and hemiazygous venous hepatic veins drain portions of the right or caudate lobes
circulations arise from the subcardinal and supracardinal of the liver. In about 3% of the population, blood from
vessels. the right lobe of the liver empties primarily through a
501
502 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
16. INFERIOR VENA CAVA 503
A B
join the intrahepatic venous complex. IVC interruption subclavian veins. Alternatively, blood may be redirected
is found in 0.6% of autopsy specimens but less often in through the superficial epigastric and circumflex iliac
imaging series.4,10,15 In this situation, blood flows from veins into the lateral thoracic vein and then into the axil-
the lower IVC into the azygous or hemiazygous vein lary vein. A systemic to portal venous pathway runs from
and then into the heart (Fig. 16-9). The hepatic veins the internal iliac veins through the hemorrhoidal plexus,
drain directly into the RA.2 The anomaly often is associ- then into the inferior mesenteric vein, and ultimately into
ated with congenital heart disease and with abnormali- the portal vein. Finally, superficial abdominal wall veins
ties of the spleen (i.e., asplenia or polysplenia), cardiac may communicate with paraumbilical veins that enter the
position, and abdominal situs.16,17 left portal vein.
Other exceedingly rare caval variants include double
IVC with retroaortic right renal vein and hemiazygous
continuation of the IVC, double IVC with retroaortic MAJOR DISORDERS
left renal vein and azygous continuation of the IVC,
and absent infrarenal IVC with preserved suprarenal Inferior Vena Cava Filter Placement
segment.4 for Venous Thromboembolic Disease
(Online Cases 23, 49, and 71 and Video 16-1)
Collateral Circulation A filtering device is inserted into the IVC for only one
Several alternate pathways allow blood to return to the reason: to prevent clinically relevant pulmonary embo-
heart when there is severe stenosis or occlusion of the lism (PE).19,20 However, IVC filters are not appropriate
IVC.18 The most common collateral route is the ascend- substitutes for standard medical therapy of venous
ing lumbar venous plexus (see Fig. 16-3). These vessels thromboembolic disease (VTE) in patients who are rea-
also communicate freely with an extensive vertebral ve- sonable candidates for anticoagulation (see later discus-
nous network. Blood flows cephalad through these veins sion and Chapter 15). In certain clinical situations, virtu-
into the azygous or hemiazygous systems and then into ally every knowledgeable physician would support filter
the SVC (see Fig. 16-6). placement. Still, a substantial number of experts remain
Blood from the pelvic veins also may bypass the IVC skeptical about their touted benefits (prevention of sig-
through periureteric and gonadal venous communi- nificant PE and associated reduction in mortality) and
cations. The external iliac vein can also drain through the concerned about the associated risks (namely, the possible
inferior epigastric vein; associated superficial abdominal predisposition to deep vein thrombosis (DVT) and post-
wall vessels then merge with the internal thoracic and thrombotic syndrome).21,22
16. INFERIOR VENA CAVA 505
A B C
D E
FIGURE 16-7 Duplicated inferior vena cava (IVC). A, Cavography prior to inferior vena cava filter placement did not suggest variant
anatomy, so a single filter was placed (B). By serendipity, a colleague later noted IVC duplication at the edge of an image on a lumbar spine
computed tomography study (arrow) (C). D, Left iliac venography confirms duplication and presence of large acute thrombus. E, From a
jugular approach, a second Guenther tulip filter was placed in the duplicated moiety above the thrombus.
506 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
FIGURE 16-8 Left inferior vena cava (IVC). A, T1-weighted magnetic resonance image shows IVC (arrow) to the left of the aorta at the
level of the kidneys. B, Coronal maximum intensity projection magnetic resonance angiogram shows the left IVC crossing the midline to join
the orthotopic suprarenal IVC.
A B
C
16. INFERIOR VENA CAVA 507
A B
FIGURE 16-10 Megacava. A, Venacavogram shows caval diameter greater than 29 mm (based on catheter markers). B, A Birds nest filter
was inserted.
16. INFERIOR VENA CAVA 509
B C
FIGURE 16-11 Megacava in a patient with temporary risk for venous thromboembolic disease. A, Preprocedure computed tomography
scan showed huge inferior vena cava that measured more than 30 mm in diameter (arrow). B, At left iliac venography from jugular approach,
the left common iliac vein measures about 30 mm in diameter. C, Therefore, retrievable filters were placed in the right common iliac and left
external iliac veins well above the inguinal ligament.
INFERIOR VENA CAVA ANOMALIES the IJ vein (Fig. 16-14). Extension of clot into the
Variants in IVC anatomy are sought (see earlier discus- IVC from tributaries may be a sign of occult malig-
sion). A duplicated IVC requires placement of filters in nancy (e.g., right gonadal vein thrombosis in ovarian
each moiety or suprarenal insertion of a single device neoplasms). Chronic total occlusion of the IVC possi-
(see Fig. 16-7). bly obviates the need for filter placement, although
clots still can pass through enlarged collaterals. If su-
INTRINSIC DISEASE prarenal filter placement is required, it is critical to
Filter location is influenced by the presence of intralu- identify an appropriate landing site and to be certain
minal clot, chronic mural disease, or extrinsic com- that the nondiseased caval segment is long enough to
pression. If caval thrombus is found, the filter is de- accommodate the filter without extension into the RA
posited just above the clot (when feasible) through (see Fig. 16-14).
510 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
Device Selection
Before intraluminal IVC filtration devices were developed,
operative caval interruption was achieved by ligation, sta-
pling, plication, or clipping. However, subsequent IVC
thrombosis was all too frequent.46,47 The Greenfield filter
was the first widely successful intraluminal device,
placed initially by open surgery and beginning in 1984 by
percutaneous means.48,49
At present, a variety of permanent IVC filters are com-
mercially available24 (Figs. 16-15 and 16-16 and Table 16-1).
The critical properties of filters are clot-trapping efficiency,
IVC and access vein occlusion rates, tendency for migra-
tion or embolization, mechanical integrity, and ease of
placement. Despite decades of experimental and clinical
studies comparing their relative merits (clot trapping
ability vs. caval thrombosis rate), none of the currently
used devices holds an unequivocal advantage.20,24,50-55
Certain filters seem to possess superior clot-trapping
ability compared with the others.55-58 This attribute may
be associated with higher rates of caval thrombosis, but
it may make these devices more suitable for patients
who cannot tolerate even small pulmonary emboli.
The more recently developed products that permit dis-
continuation of IVC filtration are termed optional filters,
which fall into two categories.59 Convertible IVC filters can
FIGURE 16-13 Improper placement of inferior vena cava filter be manipulated in situ to abolish their filtering capacity;
in setting of circumaortic left renal vein. With the filter deposited
above the circumaortic moiety (straight arrow), filter thrombosis could
none is currently commercially available in the United
allow clots to pass through the renal sinus and to the lung (direction States. Retrievable IVC filters have the potential for com-
of curved arrows). plete removal. However, they are primarily approved by
16. INFERIOR VENA CAVA 511
B C D
FIGURE 16-14 Suprarenal inferior vena cava filter. A and B, Contrast-enhanced computed tomography scans show caval thrombus
(short arrow) at the level of the renal veins but a patent cava above (long arrow). From a jugular approach, venacavography confirmed
thrombus up to the level of the renal veins (C, arrow). D, A suprarenal retrievable Guenther tulip filter was inserted.
TABLE 16-1 Permanent Inferior Vena Cava Filters period of increased risk for VTE. When risks factors for
VTE resolve or when anticoagulation can be instituted
Device/Manufacturer Material Sheath
safely, the filter may be removed. Certainly, a young,
Birds nest (Cook, Inc.) Stainless steel 12 Fr previously healthy individual who suffers major trauma
Greenfield (Boston Scientific) Stainless steel 12 Fr and VTE is an ideal candidate for a retrievable de-
Simon nitinol (Bard, Inc.) Nitinol 7 Fr vice.64,65 In fact, it might seem that having the option of
TrapEase (Cordis Corp.) Nitinol 6 Fr
Vena-Tech LP (B. Braun) Phynox 7 Fr
filter removal is ideal for all patients. However, the
evaluative period of optional filters is short compared
with the decades-long experience with permanent de-
vices. Thus, at present, if filter removal seems unlikely, a
American and European regulatory agencies for permanent permanent device should be strongly considered.66
placement.
Table 16-2 lists and Fig. 16-17 shows currently available Insertion Technique
optional IVC filter designs.60,61 Again, none of these retriev- IVC filters usually are deployed from the right IJ vein or
able devices has emerged as clearly superior to the others. a CFV. The IJ approach has several advantages (Box 16-4).
However, before selecting a particular filter, operators In the unusual circumstance in which both femoral and
are cautioned to review the most recent data regarding IJ veins are occluded or unavailable, an antecubital, up-
postplacement filter migration and long-term integrity. per arm, or external jugular vein route can be used.67
Early versions of some optional filters had serious design Box 16-2 outlines indications for suprarenal IVC filter
flaws that required their removal from the market. placement.24,68-70 Suprarenal insertion is recommended
Box 16-3 outlines the typical scenarios that favor use in pregnant women to avoid compression of the device
of a retrievable filter.62-64 For the most part, this group by the gravid uterus and to prevent PE if ovarian vein
includes patients with a limited and fairly predictable thrombosis develops.
512 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B C D
E F G H
FIGURE 16-15 Frontal and aerial views of inferior vena cava filter designs. A and B, Stainless-steel Greenfield filter (Boston Scientific,
Natick, Mass.). C and D, Birds nest filter (Cook Inc., Bloomington, Ind.). E and F, Vena-Tech LGM filter (B. Braun, Evanston, Ill.). G and
H, Simon nitinol filter (Bard, Inc., Tempe, Ariz.).
16. INFERIOR VENA CAVA 513
A B C
FIGURE 16-16 Frontal and aerial views of newer inferior vena cava filter designs. A and B, Low-profile Vena-Tech LP (B, Braun). C, TrapEase
filter (Copyright Cordis Corp.)
Guenther-Tulip Conichrome 7 Fr (J) Conical design, four hooked legs join at apex, four looped
(Cook, Inc.) wires form tulip trap
8.5 Fr (F)
Celect (Cook, Inc.) Conichrome 7 Fr (J) Eight arms replace four looped wires for improved center-
ing and retrievability
G2, G2X, Eclipse (Bard, Inc.) Nitinol 7 Fr Six arms, six legs diverge from apex, two filtering levels
G2X can be removed without separate cone device, elastic
hook lengthens retrieval period
OptEase (Cordis, Corp.) Nitinol 6 Fr Retrievable version of TrapEase device
Requires femoral retrieval, hook at bottom
ALN (Implants SS alloy 7 Fr Six upper legs with hooks
Chirurgicaux) Three lower legs facilitate device centering
Option (Angiotech) Nitinol 6.5 Fr Six radiating struts
A B
FIGURE 16-17 Retrievable inferior vena cava filters. A and B, Guenther-Tulip filter (Courtesy of Cook, Inc.).
Continued
514 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
C D
E F
G
FIGURE 16-17, contd C and D, OptEase filter (Copyright Cordis Corp., 2011). E, Eclipse filter (Courtesy of Bard, Inc.). F, Celect filter
(Courtesy of Cook Medical, Inc.). G, Guenther tulip filter with tri-lobed snare around retrieval hook (Courtesy of Cook Medical, Inc).
16. INFERIOR VENA CAVA 515
Bedside placement of IVC filters with intravascular resheathed and repositioned if being inserted
ultrasound guidance has become quite popular in with a jugular vein approach.
some centers. This approach may be especially ad- Filter is tilted more than 15 degrees off axis.74-76
vantageous in unstable patients confined to the inten- There is conflicting evidence regarding the clinical
sive care unit.71-73 On occasion, however, the lack of significance of major filter tilt with respect to clot
fluoroscopic confirmation leads to malplacement of trapping ability.77,78 The major problem with filter
the device (e.g., in an iliac vein; Fig. 16-18). asymmetry is that the retrieval process may be
The precise steps in filter deployment vary with impeded or precluded if the retrieval hook be-
each device. Several problems that may occur during comes firmly embedded in the caval wall. As such,
deployment are common to multiple devices. maneuvers to reposition the filter in line with the
caval axis (both in frontal and lateral projections)
Filter deploys more than 1 cm from intended are advocated by many experienced practitioners.
position. If the filter is of a retrievable type Filter expansion is markedly asymmetric. The
(except the OptEase model), the device can be impact of leg asymmetry on recurrent PE is
F A C T O R S F AV O R I N G A D VA N T A G E S O F R I G H T
R E T R I E VA B L E I N F E R I O R INTERNAL JUGULAR
V E N A C AVA F I LT E R APPROACH FOR INFERIOR
PLACEMENT V E N A C AVA F I LT E R
PLACEMENT
Young patient
Prophylaxis after major trauma, in intensive care Lower frequency of access site thrombosis
unit setting, or before high-risk operations Ability to reposition some retrievable devices if
During lower extremity deep vein thrombolysis, initial expansion is suboptimal
especially with inferior vena cava involvement Possibly better control of filter orientation
During pregnancy Avoidance of failed opening and migration
Necessary in presence of infrarenal inferior vena
cava thrombus
A B C
FIGURE 16-18 Malplacement of inferior vena cava (IVC) filter based on intravascular ultrasound guidance alone. Filter was inadvertently placed
in the left iliac vein. The retrieval hook was captured with a snare device (A), withdrawn into a guiding sheath (B), and repositioned in the IVC (C).
516 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
controversial.78,79 However, some intervention- TABLE 16-3 Complications from Inferior Vena Cava Filter
alists attempt to improve the leg orientation or Placement
filter axis if it is grossly asymmetric, even though Event Frequency (%)
this practice is not recommended by the manufac-
turers or some experts.24,80 Access site thrombosis 0-6
Recurrent deep vein thrombosis 21
Filter fails to open at all. If still attached to the
Inferior vena cava thrombosis 0-30
delivery cable, it should be withdrawn into the Inferior vena cava perforation (almost always 0-41
sheath and removed. If not, the capture hook is inconsequential)
carefully engaged with a snare device and the Filter migration (almost always inconsequential) 3-69
filter removed. Actual manipulation of an unex- Filter embolization "1
Filter fracture 2-10
panded filter poses some risk for central emboli-
Dislodgement or entrapment by catheters or "1
zation to the heart.81 guidewires
Other complications 4-11
Bleeding, hematoma
Results Pneumothorax
Arteriovenous fistula
Using fluoroscopic guidance, IVC filters (permanent
Air embolism (to right heart chambers)
or optional) can be placed successfully in almost every Stroke (from paradoxical embolism of air or clot)
instance.23,24,61,82-90 Technical failures are usually related Failed deployment
to unsuspected caval disease that precludes or obviates IVC stenosis
the need for a filter. Infection
It is disappointing that almost three decades after the
first report of percutaneous placement of an IVC filter,
there is not indisputable evidence for their efficacy and A most concerning though hotly debated liability of
safety in preventing PE in certain populations. Only one IVC filters insertion is the reported excess risk of subse-
well-recognized randomized study has addressed this quent lower extremity post-thrombotic syndrome re-
issue.91 The large multicenter PREPIC trial showed that lated to DVT (reported in 11% to 13% of procedures).102
permanent IVC filters significantly reduce the risk for At the extreme end of the spectrum, complete IVC
PE in patients with documented proximal DVT with- thrombosis is a serious and potentially life-threatening
out significant effect on mortality, but at the price of event (Fig. 16-19). The frequency of this occurrence falls
increased rates of leg DVT at 8 years.21,36 Still, multiple in the 1% to 12% range.95,103-105 There are conflicting data
large (though uncontrolled) clinical series show a fairly regarding the relative rates of filter thrombosis with
consistent 2% to 7% filter failure rate (i.e., new clinically the various devices.97,106,107 In patients with profound
significant PE after placement) among the various per- or life-threatening symptoms from IVC thrombosis
manent and retrievable models.75,92-98 The risk for subse- (e.g., phlegmasia cerulea dolens), catheter-directed
quent fatal PE after an IVC filter is inserted is estimated thrombolysis may be indicated108,109 (see Chapter 15).
at about 0.7%.24 Suprarenal filter placement seems to be Minor filter migration ("1 to 2 cm) is usually of little
as effective and safe as infrarenal deployment.40 consequence. Significant permanent device migration
Recurrent pulmonary emboli have several causes, after image-guided placement has been reported but is
including device failure, propagation of thrombus above far less common than malplacement from inadequate or
the filter, and embolization from other sources (e.g., up- nonexistent imaging during insertion110-112 (see Fig. 16-18).
per extremity, gonadal or renal vein). Some patients On the other hand, the very properties that allow re-
may require anticoagulation or, rarely, placement of an trievable filters to be removed make them more prone to
additional filter. movement. In fact, several early filter designs were re-
moved from the market because of late occurrence of
central embolization. Migration has been reported from
Complications cardiopulmonary resuscitation and inadvertent guide-
Table 16-3 outlines immediate and long-term complica- wire entrapment (see Fig. 18-21). It has been postulated
tions of IVC filter placement.23,24,82-101 The major compli- that some cases of filter motion occur when a large em-
cation rate is about 0.3%. Less than 0.2% of patients die bolus suddenly hits the filter, causing acute obstruction;
as a direct result of the procedure. Adverse outcomes are the markedly elevated IVC pressure forces the filter to
comparable with suprarenal and infrarenal placement.40 move centrally.113,114
Access site thrombosis is the most common untoward Although embolization of all or part of an IVC filter to
event after caval filter insertion (about 5% of cases with the heart or pulmonary artery is quite rare, the event is
currently available sheath systems). However, it is rarely potentially lethal.115-118 If an IVC filter becomes lodged in
symptomatic. the heart, arrhythmias, tricuspid valve injury, pericardial
16. INFERIOR VENA CAVA 517
A B
tamponade, or acute myocardial infarction can result. duplex ultrasound (US) of the lower extremities
Transvenous retrieval or repositioning has been per- exclude DVT?
formed successfully with a variety of techniques, includ- 4. Is the patient expected to live more than
ing use of a large sheath system and looped guidewire or 6 months?
snare techniques117,119-121 (see Chapter 18).
If the answer to any of these questions is no,
Filter fracture/fragmentation is more problematic
then the filter should not be removed at that time.
with some retrievable models. This complication has
Further clinical workup or medication adjustment is
been reported in about 2% to 4% of cases.76,98 Penetration
warranted.
of the caval wall by device legs or hooks is very common
Retrieval is safe even during therapeutic anticoagu-
but rarely consequential101 (see Fig. 16-19). However,
lation provided the INR does not exceed about 3.0.124
perforation into various neighboring structures (e.g.,
The feasibility of filter removal is largely a function
aorta, bowel, ureter, pancreas) can be problematic.100,122,123
of dwell time and the presence of residual thrombus
within the filter125,126 (Table 16-4). If embolic protection
Inferior Vena Cava Filter Retrieval is likely needed for longer than the accepted dwell time
(Video 16-2 and Online Case 38) of the filter, the interventionalist can periodically cap-
Patient Selection ture the device and reposition it within the recovery
sheath to a slightly different location in the IVC.127
A patient is considered for retrievable IVC filter removal
Some retrievable filters can be removed safely after
when the risk for PE is low, either because underlying
much longer periods than recommended by the manu-
risk factors for VTE have resolved or because the patient
facturers, although the safety of this maneuver cannot
is finally undergoing anticoagulant therapy. In addition,
be guaranteed.65,82,128-130
filter removal is advisable if the local standard-of-care
demands lifelong anticoagulation by virtue of filter pres- Technique
ence.59,60 The following questions should be asked:
With the exception of the OptEase device, filter retrieval
must be done through the IJ vein. Venacavography is
1. Is there no reason to expect progression of DVT
necessary to identify thrombus within or extending
since filter placement, new development of VTE,
above the filter. A pigtail (or similarly shaped) catheter
or near future return of risk factors for VTE?
2. If anticoagulation is underway, have appropriate
therapeutic levels been achieved, patient tolerance TABLE 16-4 Manufacturers Guidelines for Inferior Vena
confirmed, and no complications observed for Cava Filter Removal
at least 1 week (preferably 2 to 3 weeks)? For
individuals receiving warfarin anticoagulation, Percentage of Thrombus
Filter Allowing Removal Access Site
an international normalized ratio (INR) should
be obtained within several days of the planned Guenther-Tulip/ "25% of cone Jugular
procedure (typical target range is 2.0 to 3.0). Celect
G2, Eclipse No recommendation Jugular
3. If the filter was placed for prophylactic reasons
Optease No recommendation Femoral
without a diagnosis of VTE, does a recent
518 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
A B C
FIGURE 16-22 Trapped thrombus within IVC filter precludes removal (A). Patient returned about 1 month later on anticoagulation,
at which time complete clot lysis has occurred (B). Nonetheless, the filter legs would not entirely release from the caval wall (C), and the
device was left in place permanently.
long 10- to 12-Fr sheath (see Fig. 16-17G). Once the snare chest to locate remaining filter fragments that may
is cinched down on the hook securely, the sheath is then themselves require removal.
slid over the filter, compressing the legs and disengag-
ing the device from the caval wall. In most cases, re- Results and Complications
trieval is straightforward. Among published series, the removal rate for retriev-
However, if the retrieval hook abuts or becomes able filters ranges from 78% to 100%.* The most com-
embedded into the vascular wall, extraction may be mon reasons for failure are the presence of substantial
quite challenging (Fig. 16-23). A variety of methods have thrombus within the filter (precluding safe withdrawal),
been devised to remove stubborn filters131-142 (Fig. 16-24 inability to engage the retrieval hook, and permanent
and Box 16-5). Even with extraordinary effort, capturing incorporation into the IVC wall. Although filter re-
the filter apex and removing the filter may be impossi- trieval becomes more challenging as the dwell time
ble. Considerable force or complex manipulations may increases, some filters can be removed many months
be needed to release some filters from the cava. In the beyond the manufacturers suggested period.130,135,145,148
process, however, the filter may become grossly dis- IVC filter extraction is a remarkably safe procedure.
torted with the potential for caval thrombosis, gross fil- Despite some almost heroic maneuvers used to retrieve
ter leg perforation of vital structures, or embolization of stubborn filters, serious complications are extremely
filter fragments to the heart (Fig. 16-25). rare. Some early, creative methods of retrieval were as-
Many interventionalist do not bother with postre- sociated with significant risk of partial caval thrombosis.
trieval cavography unless the removal was difficult or With modifications of these techniques, most injuries to
the patient experienced severe pain. Most residual inti- the caval wall are self-limited.124,133,135 Still, the filter can
mal flaps or adherent thrombi that are detected require become markedly distorted during an unsuccessful at-
no specific treatment. Frank IVC perforation with ex- tempted withdrawal, which can predispose to IVC
travasation demands careful monitoring or direct treat- thrombosis, perforation of adjacent structures, or filter
ment. The operator should examine the integrity of the fragmentation.
device. Evidence of missing elements should prompt
careful fluoroscopic examination over the abdomen and *See references 61, 65, 82, 84-90, 101, 104, 107, 127, 130, 143-147.
520 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
A D VA N C E D T E C H N I Q U E S C AU S E S O F O B S T R U C T I O N
F O R I N F E R I O R V E N A C AVA OF THE INFERIOR VENA
F I LT E R R E T R I E VA L C AVA
A B C
D E
FIGURE 16-24 Loop snare technique for difficult inferior vena cava filter retrieval. A, Patient had required bilateral common iliac veins filters.
B, The right-sided filter was easily snared and removed. The hook on the left-sided filter could not be engaged. Therefore, a guidewire was advanced
around the embedded filter hook. The end of the wire loop was captured with a snare placed in tandem through the vascular sheath (C, arrow). The
end of the wire was brought up through the sheath and out the body, allowing significant force to be applied to the filter apex. The sheath was passed
down over the filter hook and onto the apex (D), and the device was pulled into the sheath (E) and ultimately out of the patient.
522 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
Imaging Treatment
CROSS-SECTIONAL TECHNIQUES MEDICAL THERAPY
IVC thrombosis is usually diagnosed by CT or MR The major goals of treatment are to prevent PE, limit clot
angiography or by color Doppler sonography.9,155,156 propagation that may cause renal vein and hepatic vein
On contrast-enhanced CT, the IVC is enlarged, and col- thrombosis, and potentially avoid the post-thrombotic
lateral vessels may opacify. A low-density filling defect syndrome (see Chapters 1 and 15). First-line manage-
is seen (see Fig. 16-19). At first glance, heterogenous ment for IVC thrombosis is anticoagulation following
enhancement of the lumen (from mixing of unopaci- the guidelines for lower extremity DVT.158 However, this
fied blood) can mimic intraluminal clot in the early regimen is contraindicated in certain cases, including in
phases of dynamic CT scanning.157 Intraluminal exten- patients with risk factors for bleeding from anticoagu-
sion of tumor thrombus (typically from renal cell or lants and those who have had a previous adverse reac-
hepatocellular carcinoma and typically heterogeneous tion to heparin or warfarin. In such circumstances,
in appearance) can mimic bland IVC thrombosis (see placement of a suprarenal IVC filter may be appropriate
Fig. 10-33 and Fig. 16-26). (see earlier discussion).
16. INFERIOR VENA CAVA 523
B C
ultimately extend outside or into the lumen of the cava.9 showing intermediate signal intensity on T1-weighted
Extraluminal growth of vascular leiomyosarcoma hap- sequences and increased signal on T2-weighted se-
pens in most cases; intraluminal extension alone is seen quences. The lower one third of the vena cava is least
in about one fourth of patients. The segment from often involved.9,167,168 It is often impossible to differen-
the renal veins to the hepatic veins is most frequently tiate primary caval leiomyosarcoma from the more
involved.167 common retroperitoneal leiomyosarcoma.
A B
FIGURE 16-27 Leiomyosarcoma of the inferior vena cava (IVC) on contrast-enhanced computed tomography in one patient (A) and on
venacavography in another (B). In the latter case, the nonocclusive mural tumor mimics bland thrombus.
16. INFERIOR VENA CAVA 525
BOX 16-7
C AU S E S O F N A R R O W I N G
OF THE INFERIOR VENA
C AVA
Extrinsic compression
Right common iliac artery
Right renal artery
Vertebral column
Hepatic masses
Ascites
Hepatomegaly
Pregnancy
Retroperitoneal masses (e.g., tumor, hematoma)
Aortic ectasia or aneurysm FIGURE 16-28 Massive hepatocellular carcinoma produces
extrinsic compression of the intrahepatic inferior vena cava.
After liver transplantation
Wall thickening from resolved thrombotic disease
Inferior vena cava filter
Profound hypotension or hypovolemia oversized stents (about 50% larger than measured
(flat IVC) nominal diameter) are routinely chosen.
Retroperitoneal fibrosis
Functional obstruction (e.g., Valsalva maneuver)
Retroperitoneal Fibrosis
Retroperitoneal fibrosis is a rare, poorly understood chro-
nic inflammatory disorder of the abdomen and pelvis.
right renal artery (on the posterior cava), or the spine Genetic and autoimmune origins have been proposed; in
(see Fig. 15-6). The IVC can appear severely narrowed a few cases, it is the result of tumor, infection, or chronic
if the patient performs a vigorous Valsalva maneuver use of certain drugs, such as ergot derivatives.184 The in-
during imaging. The most frequent reason for patho- filtrative fibrotic process often extends from the level of
logic extrinsic compression is liver disease (e.g., severe the kidneys into the pelvis. Symptomatic involvement of
hepatomegaly, caudate lobe enlargement, hepatic the IVC occurs in only 2% of cases.
masses, massive ascites) (Figs. 16-28 and 16-29). Large CT or MRI reveals encasement of the IVC and iliac
abdominal aortic aneurysms (AAA) also may efface the veins185,186 (Fig. 16-32). In symptomatic patients, the cava
vena cava, and severe obstruction of the IVC by an may be completely obliterated. The inflammatory tissue
AAA can lead to caval thrombosis.178 Mural thickening often involves other central retroperitoneal structures,
from resolved thrombosis can leave mild or moderate including the aorta, ureters, and small bowel.
caval narrowing. Focal caval obstruction in the set-
ting of orthotopic liver transplantation is discussed in
Chapter 12.
Membranous Obstruction
Intravascular stents are placed for certain IVC ob- Membranous obstruction of the IVC describes a related set of
structions. Most often, stents are used for palliative conditions in which a fibromuscular membrane develops
relief of malignant IVC obstruction (e.g., hepatocellu- within the IVC just below the RA (type 1) or a fibrous band
lar carcinoma), after orthotopic liver transplantation, completely replaces the intrahepatic IVC for a variable
and for membranous IVC obstruction.179-183 Gianturco distance (type 2).187 Central hepatic vein involvement is
Z-stents and Wallstents have been used (among others) common. The etiology is unknown. Membranous IVC
for this purpose (Fig. 16-30 and see Fig. 12-39). Return obstruction is most commonly seen in India, Japan, Korea,
of near normal caval blood flow is accomplished in the China, and South Africa. In those countries, it is the lead-
majority of cases; the IVC usually remains patent for ing cause of Budd-Chiari syndrome (BCS), with a slowly
the remainder of the patients life. Placement of stents progressive course rather than the fulminant disease of
in the IVC, particularly near the heart, can be treacher- thrombotic BCS that is typical in Western nations.188
ous (Fig. 16-31). The major risk of IVC stent placement The diagnosis is made by cross-sectional imaging.189,190
is immediate or delayed migration into the heart, The radiographic appearance is variable, ranging from
which can have disastrous consequences. Therefore, a discrete bandlike obstruction to long segment complete
526 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
FIGURE 16-29 Extrinsic compression of the intrahepatic inferior vena cava (A, arrows). This patient with thalassemia had
extramedullary hematopoiesis about the spine on T1-weighted magnetic resonance images (B). Note high signal intensity in the paraspinal
masses and the vertebra.
A B
16. INFERIOR VENA CAVA 527
A B C
FIGURE 16-31 Stent migration during treatment of inferior vena cava (IVC) stenosis. A, Venacavography after liver transplant shows a
significant intrahepatic stenosis. B, A Wallstent was placed at the site and dilated with a balloon. Movement of the upper end towards the
right atrium is evident (arrow). After removing the balloon, the stent migrated completely into the heart but remained around the guidewire.
C, The stent was ultimately snared and removed through the jugular vein.
event or secondary to infection or trauma (e.g., lumbar exploratory laparotomy because they are hemodynami-
spine surgery).193-195 The classic clinical triad is local- cally unstable or show evidence of bleeding on peritoneal
ized pain, a palpable aneurysm, and an abdominal lavage or imaging. With blunt abdominal trauma, the
bruit. The diagnosis is made by sonography, CT angi- most common site of laceration is the retrohepatic portion
ography, or MR angiography (see Fig. 7-12). The com- of the IVC.
munication most frequently develops between the
distal aorta and IVC. Stent grafts have been used to seal
Aneurysms
these connections.196,197
Aneurysms of the IVC are exceedingly rare.199-201 Many
remain asymptomatic for years. They may only come to
Trauma medical attention after complete thrombosis or PE. IVC
Injury to the IVC may result from blunt or penetrating aneurysm can mimic IVC occlusion from other causes.
trauma to the abdomen or chest198 (Fig. 16-33). Most pa- Surgical treatment requires partial or complete excision
tients who initially survive the event undergo immediate of the aneurysm.
B C
FIGURE 16-33 Inferior vena cava (IVC) disruption from motor vehicle crash. Contrast-enhanced computed tomography scans
(A and B) show disruption of the IVC (arrow). The findings were confirmed at venacavography (C).
16. INFERIOR VENA CAVA 529
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tulip vena cava filter through a femoral vein approach. J Vasc Interv bosis. Cardiovasc Revasc Med 2008;9:36.
Radiol 2005;16:391. 163. Wotkowicz C, Wszolek MF, Libertino JA. Resection of renal tumors
139. Hagspiel KD, Leung DA, Aladdin M, et al. Difficult retrieval of a invading the vena cava. Urol Clin North Am 2008;35:657.
Recovery IVC filter. J Vasc Interv Radiol 2004;15:645. 164. Kanematsu M, Imaeda T, Minowa H, et al. Hepatocellular carci-
140. Contractor S, Bhagat N, Mahmood Y, et al. Retrieval of a tilted noma with tumor thrombus in the inferior vena cava and right
Guenther tulip filter with the superior hook embedded in the atrium. Abdom Imaging 1994;19:313.
caval wall. J Vasc Interv Radiol 2007;18:1455. 165. Kieffer E, Alaoui M, Piette JC, et al. Leiomyosarcoma of the inferior
141. Ullman JM. Technique for snaring an inaccessible Guenther tulip vena cava: experience in 22 cases. Ann Surg 2006;244:289.
filter. J Vasc Interv Radiol 2006;17:1067. 166. Hollenbeck ST, Grobmyer SR, Kent KC, et al. Surgical treatment
142. Yamagami T, Kato T, Nishimura T. Successful retrieval of a Guen- and outcomes of patients with primary inferior vena cava
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introducer. J Vasc Interv Radiol 2005;16:1760. 167. Kyriazi MA, Stafyla VK, Chatzinikolaou I, et al. Surgical chal-
143. Stein PD, Alnas M, Skaf E, et al. Outcome and complications of lenges in the treatment of leiomyosarcoma of the inferior
retrievable inferior vena cava filters. Am J Cardiol 2004;94:1090. vena cava: analysis of two cases and brief review of the literature.
144. Doody O, Given MF, Kavnoudias H, et al. Initial experience in 115 Ann Vasc Surg 2010;24:e13.
patients with the retrievable Cook Celect vena cava filter. J Med 168. Jenkins S, Marshall GB, Gray R. Leiomyosarcoma of the inferior
Imaging Rad Oncol 2009;53:64. vena cava. Can J Surg 2005;48:252.
145. Looby S, Given MF, Geoghagen T, et al. Gunther tulip retrievable 169. Hallscheidt PJ, Fink C, Haferkamp A, et al. Preoperative staging
inferior vena caval filters: indications, efficacy, retrieval, and com- of renal cell carcinoma with inferior vena cava thrombus using
plications. Cardiovasc Intervent Radiol 2007;30:59. multidetector CT and MRI: prospective study with histopatho-
146. Cantwell CP, Pennypacker J, Singh H, et al. Comparison of the logical correlation. J Comput Assist Tomogr 2005;29:64.
recovery and G2 filter as retrievable inferior vena cava filters. 170. Sheth S, Scatarige JC, Horton KM, et al. Current concepts in the
J Vasc Interv Radiol 2009;20:1193. diagnosis and management of renal cell carcinoma: role of mul-
147. Keller IS, Meier C, Pfiffner R, et al. Clinical comparison of two tidetector CT and three-dimensional CT. Radiographics 2001;
optional vena cava filters. J Vasc Interv Radiol 2007;18:505. 21:S237.
148. Marquess JS, Burke CT, Beecham AH, et al. Factors associated 171. Cuevas C, Raske M, Bush WH, et al. Imaging primary and second-
with failed retrieval of the Guenther tulip inferior vena cava filter. ary tumor thrombus of the inferior vena cava: multi-detector com-
J Vasc Interv Radiol 2008;19:1321. puted tomography and magnetic resonance imaging. Curr Probl
149. Joshi A, Carr J, Chrisman H, et al. Filter-related, thrombotic occlu- Diagn Radiol 2006;35:90.
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J Vasc Interv Radiol 2003;14:381. germ cell carcinoma: diagnosis via endovascular biopsy and a
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vena cava involvement different? J Urol 2004;171:588. coma versus leiomyomatosis: difficult diagnosis. J Vasc Surg 2002;
151. Okuda K. Membranous obstruction of the inferior vena cava. 36:1256.
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152. Kaushik S, Federle MP, Schur PH, et al. Abdominal thrombotic rior vena cava for hepatic malignancy. Am Surg 2001;67:1081.
and ischemic manifestations of the antiphospholipid antibody 175. Blute ML, Leibovich BC, Lohse CM, et al. The Mayo Clinic experi-
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153. Hausler M, Hubner D, Delhaas T, et al. Long term complications patients with renal cell carcinoma and venous tumour thrombus.
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154. Gargiulo III NJ, OConnor DJ, Veith FJ, et al. Long-term outcome 176. Ito H, Hornick JL, Bertagnolli MM, et al. Leiomyosarcoma of
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155. Sheth S, Fishman EK. Imaging of the inferior vena cava with 177. Cho SW, March JW, Geller DA, et al. Surgical management of
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defects on CT and MRI. AJR Am J Roentgenol 2005;185:717. stents: clinical experience in the vena cava and large veins. Cardio-
158. Bates SM, Ginsberg JS. Treatment of deep-vein thrombosis. New vasc Intervent Radiol 1992;15:328.
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16. INFERIOR VENA CAVA 533
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C H A P T E R
17
Upper Extremity Veins and
Superior Vena Cava
Karim Valji
ANATOMY onto the upper surface of the axillary vein (Fig. 17-3).
The deep veins of the forearm follow the radial and
ulnar arteries. They unite and then divide at the elbow
Development to form paired brachial veins. These vessels run along-
In the embryo, the upper limb buds are drained by side the brachial artery and then join the basilic vein to
marginal veins.1 The deep veins develop along with become the axillary vein.
their corresponding arteries. The preaxial and postaxial The axillary vein begins at the confluence of the bra-
portions of the marginal vein become the cephalic and chial and basilic veins. Several branches of the brachial
basilic veins, respectively. plexus course between the artery and vein in this re-
The central thoracic veins are formed from the gion. At the lateral border of the first rib, the axillary
precardinal (anterior) and common cardinal vessels1 vein becomes the subclavian vein (see Fig. 17-3). Several
(Fig. 17-1). The upper segment of the precardinal vein tributaries, including the external jugular vein, enter the
becomes the internal jugular vein. The subclavian vein subclavian vein. The vein runs in front of the anterior
enters from the arm and joins the lower portion of the scalene muscle. At the medial edge of the anterior sca-
precardinal vein. An interprecardinal anastomosis con- lene muscle, the internal jugular vein joins the subclavian
nects the two precardinal veins and develops into the vein to form the brachiocephalic (innominate) vein.
left brachiocephalic vein. The lower right precardinal The right brachiocephalic vein courses almost vertically
vein becomes the upper superior vena cava. A remnant in front of the right brachiocephalic artery. Tributaries
of the left precardinal vein becomes the left superior include the right vertebral, internal thoracic (mam-
intercostal vein. mary), inferior thyroid, and first posterior intercostal
veins. The left brachiocephalic vein (which is more than
twice as long as the right) passes inferomedially in
Normal Anatomy front of the left subclavian and left carotid arteries.
The arms are drained by superficial and deep venous Branches are comparable to those on the right with the
pathways. Numerous perforators connect these systems. addition of the left superior intercostal and thymic veins.
Unlike the lower extremities, the superficial system is In most cases, the former vessel is the continuation of
dominant. It arises from two complex venous plexuses the accessory hemiazygous vein (see Fig. 17-1). The major
on the dorsal and palmar surfaces of the hand.2 The lymphatic ducts (including the thoracic duct on the left)
cephalic and basilic veins originate from the dorsal venous enter the venous circulation near the junction of the left
network and run on the radial and ulnar sides of the subclavian and jugular veins.
forearm, respectively. The median vein of the forearm The brachiocephalic veins merge to form the superior
drains the palmar venous plexus and joins the basilic vena cava (SVC), which is valveless. The SVC enters the
vein near the elbow. The median cubital vein connects the right atrium at about the level of the third costal cartilage.
basilic and cephalic veins at the elbow (Fig. 17-2). In the The azygous vein ascends from the abdomen into chest
upper arm, the basilic vein lies medial to the biceps through the right crus of the diaphragm. It arches anteri-
muscle and forms the axillary vein at the lateral border orly to an opening in the back wall of the SVC above the
of the scapula (see Fig. 17-2). The cephalic vein runs su- right main stem bronchus (Fig. 17-4; see also Fig. 17-1).
perficial and lateral to the biceps muscle, into the delto- The main trunk of the azygous vein drains the right pos-
pectoral groove, through the infraclavicular fossa, and terior and superior intercostal veins. The hemiazygous vein
534
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 535
Cephalic vein
A B
Paired brachial veins
Basilic vein
C
FIGURE 17-2 Venous anatomy of the right arm at the elbow (A), upper arm (B), and shoulder (C).
536 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
Axillary vein
A
Superior vena cava
B
Left brachiocephalic vein Axillary vein
FIGURE 17-3 Normal right (A) and left (B) central thoracic veins.
A B
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 537
A C
B
FIGURE 17-5 Left superior vena cava (SVC). A, Chest radiograph shows left subclavian central venous catheter passing to the left
of the spine (arrow). B, Computed tomography angiogram shows left SVC (arrow). C, At a more inferior level, the left SVC enters the coronary
sinus (arrow).
A B
A B C
FIGURE 17-8 Collateral circulation with high superior vena cava (SVC) obstruction from
Hodgkin disease on coronal reformatted computed tomography angiography. A, Note filling
of the left subclavian vein and retrograde flow in the superior intercostal vein (arrow) and pericar-
diophrenic collateral. B, Retrograde filling of the azygous vein (arrow). C, Retrograde filling of the
accessory hemiazygous vein and paravertebral collaterals. D, Anterior chest wall collateral veins.
BOX 17-1
C AU S E S O F U P P E R
EXTREMITY VENOUS
THROMBOSIS
Medical devices
Vascular access devices (prior or existing)
Transvenous cardiac pacemakers
Transvenous monitoring devices
Extrinsic compression
Primary (spontaneous or effort thrombosis,
Paget-Schroetter disease)
Secondary: malignancy/adenopathy
Thoracic masses
Fibrosing mediastinitis
Thrombophilic state (see Boxes 1-4 and 1-5)
Trauma/surgery
Intravenous drug abuse
Toxic agents (e.g., chemotherapeutic drugs)
Heart failure
FIGURE 17-9 Occlusion of the superior vena cava and both Radiation therapy
brachiocephalic veins. Collateral circulation occurs primarily
through superficial chest wall veins.
540 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
with upper extremity or internal jugular DVT.17-21 Even simple and safe to perform, the sensitivity and speci-
with anticoagulation, complete recanalization of throm- ficity of ultrasound in this setting (82% in one contem-
bosed upper extremity veins is not the rule.22 Rather, porary study) are less than desirable.29 The clavicle
clots often organize over time, leaving a fibrotic lumen and sternum hide most of the central brachiocephalic
and scarred vein wall. Post-thrombotic syndrome with veins and the SVC from direct visualization. When
minor or severe functional disability follows in 7% to 46% ultrasound is negative or equivocal and clinical sus-
of cases.17,23,24 picion remains high, catheter or magnetic resonance/
computed tomography (MR/CT) venography should
Clinical Features be done.
Some patients with acute venous thrombosis are com- A thorough examination includes study of the acces-
pletely asymptomatic. Others complain of arm swelling, sible portions of the axillary, subclavian, brachioce-
pain, cyanosis, coolness, and distended superficial veins. phalic, and internal jugular veins; peripheral upper
These symptoms can mimic infection, lymphatic obstruc- arm veins are occasionally interrogated. Color Doppler
tion, or blunt trauma. With chronic venous occlusion, imaging detects stenoses, occlusions, and collateral
arm fatigue after exercise may be experienced. In less channels, and Doppler waveform analysis is added
than 5% of patients (most of whom have an underlying to identify physiologic signs of more central obstruc-
malignancy), widespread venous thrombosis leads to tion. Normally, a triphasic atrial waveform with super-
the syndrome of phlegmasia cerulea dolens and arterial imposed respiratory variation is present (Fig. 17-10).
insufficiency.25,26 The typical patient with Paget-Schroetter Absent or monophasic waveforms or asymmetry
disease is a young person complaining of the sudden between sides may be a clue to central obstruction.30
onset of arm swelling and pain. A history of vigorous The subclavian vein dilates with a Valsalva maneuver
physical activity (e.g., weight lifting) can often be elicited. and collapses with rapid inspiration (i.e., sniff test).
Indwelling venous catheters do not seem to alter the
accuracy of the technique.31
Imaging
Signs of venous thrombosis include an intralumi-
CROSS-SECTIONAL TECHNIQUES nal filling defect, absent flow, or an abnormal Doppler
Color Doppler sonography is the first-line imaging tool tracing (Fig. 17-11). The latter finding can be confirmed
for detecting axillosubclavian and central venous ste- with contrast venography. Thrombosis can be missed for
nosis and thrombosis.27,28 Even though ultrasound is several reasons.
B
FIGURE 17-10 Duplex sonography of the subclavian veins.
A, Normal spectral tracing with reflected atrial activity and superim-
posed respiratory variation. B, Abnormal flat tracing suggests a more FIGURE 17-11 Partial thrombosis of the right internal jugular
central occlusion. In this case, the brachiocephalic vein was occluded. vein is identified by color Doppler sonography.
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 541
A B C
D E
FIGURE 17-12 Thoracic outlet syndrome with subclavian vein thrombosis. A, Right basilic venography shows the basilic and axillary
veins are patent. There is abrupt occlusion of the mid portion of the right subclavian vein. Of note, collateral circulation beyond this point
is sparse. Faint opacification of the right brachiocephalic vein is observed (arrow). The occlusion was crossed with a guidewire. Tissue
plasminogen activator was infused at 1 mg/hr overnight through a multiside hole catheter. Complete resolution of clot with normal antegrade
blood flow has been accomplished (B). There is mural or extrinsic narrowing of the central right subclavian vein (arrow). In this case, the site
of extrinsic compression was dilated with a 14-mm ! 4-cm angioplasty balloon (C). Patient underwent surgical release of the costoclavicular
space and first rib resection. Six-month follow-up venography reveals excellent flow through the central veins with only minimal residual
narrowing (D). However, with extreme arm abduction, near-occlusive compression of the subclavian vein occurs (E).
542 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
indwelling central venous devices may require catheter in the upper extremity and torso include deformity and
removal or long-term anticoagulation. rethrombosis from extrinsic compression, in-stent re-
stenosis, stent migration, shortening or fracture, and
ENDOVASCULAR AND OPERATIVE THERAPY jailing of important tributaries such as the internal
More aggressive transcatheter interventions are appro- jugular vein.44
priate for: Short-term results of thrombolysis with or without
mechanical thrombectomy devices are excellent in
Poor response to medical treatment with severe
about 75% to 85% of cases; thrombolysis is clearly supe-
persistent symptoms
rior to anticoagulation alone for reestablishing flow in
Suspected spontaneous (effort) thrombosis
fresh occlusions.43,45-47 Late reocclusion is a common
Widespread venous occlusion (phlegmasia
problem, particularly when the underlying cause of
cerulea dolens)
thrombosis (e.g., indwelling catheter, thrombophilic
For acute venous thrombosis (less than 10 to 14 days), state, extrinsic compression) is not eliminated. How-
enzymatic fibrinolysis with or without adjunctive ever, the evidence is weak with respect to the long-term
mechanical thrombectomy devices are favored.38 If benefit of catheter-directed thrombolysis compared
a central venous catheter or device is present, it is with therapeutic anticoagulation for prevention of up-
preferable to remove it. However, patients who are per extremity post-thrombotic syndrome.47
dependent on such catheters may have them left in For subacute and chronic venous thrombosis (more than
place. Although systemic infusion can be used, the 10 to 14 days), primary angioplasty with or without
preferred method is catheter-directed local throm- stent placement is recommended (Fig. 17-13). Given
bolysis (see Fig. 17-12) (see Chapter 3 for technical their general unresponsiveness to fibrinolytic agents,
details). Access is usually gained through an ipsilat- clinical benefit from thrombolysis in this situation
eral basilic or brachial vein. If necessary, the common is low compared with the risks entailed. Chronic orga-
femoral or internal jugular vein may be used. The nized occlusions can be difficult to cross. If antegrade
patient and operator should understand that complete traversal is impossible, retrograde entry from the
therapy may require several days of infusion and common femoral vein may be successful. When stan-
relatively large doses of fibrinolytic agents. Mechani- dard guidewires and catheters fail, the back end of a
cal thrombectomy devices often serve as adjuncts to hydrophilic wire can be tried. Finally, sharp recanali-
chemical lysis.39 zation with the catheter and stylet from a transjugular
Patients are vigorously anticoagulated during the intrahepatic portosystemic shunt set may be fruitful.48,49
procedure and often require long-term anticoagulation. These latter maneuvers should be done knowing the
Underlying stenoses are treated with balloon angio- risks of entering major arteries nearby. If a cosmetically
plasty. The role of stents in this setting is controver- satisfying result is obtained from angioplasty alone,
sial.40-42 They are generally avoided in thoracic outlet some interventionalists will then recommend at least
syndrome, although some reports claim good long- short-term anticoagulation. In many instances, how-
term results after stent placement.43 Stents are used ever, intravascular stent placement is deemed necessary
very judiciously in other cases. The drawbacks of stents to maintain patency.50
A B
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 543
For primary axillosubclavian thrombosis (venous thoracic device selection and insertion are given in Chapter 16.
outlet syndrome), an integrated approach that combines The selected filter must be oriented with the apex toward
catheter-directed therapy with surgery is now thoroughly the heart. For example, the jugular version of asymmetric
embraced by many experts (see Fig. 17-12). The standard filters must be used from the femoral approach. Superior
algorithm includes the following features43,51-57: venacavography is done to ensure proper positioning and
adequate caval length to accommodate the device.
Immediate anticoagulation
In the United States, SVC filter placement currently
Prompt catheter-directed thrombolysis as initial
represents an off-label use of these devices. Long-term
treatment (for acute occlusion)
follow-up is limited. Nonetheless, there is some evi-
Angioplasty if flow-limiting obstruction is found;
dence to support the intervention (prevention of pul-
stents should be avoided
monary embolism, low frequency of filter migration or
A course of anticoagulation with warfarin
SVC thrombosis.)61 Still, there is a very small but real
(Coumadin)
risk for potentially devastating complications from
Medical therapy if no extrinsic compression is
strut perforation into adjacent structures, including
detected after thrombolysis
pericardial tamponade, bleeding from aortic laceration,
Immediate or delayed surgical decompression
and tension pneumothorax.61-63 These events do not
(e.g., first rib resection and subclavius tendon
occur with inferior vena cava (IVC) filters.
release with patch venoplasty, bypass, or
external venolysis) for axillary or subclavian
vein compression detected after thrombolysis Upper Extremity Venous Stenoses
Angioplasty (with or without stent placement) or (Online Case 93 and Video 17-1)
surgery for residual postoperative stenoses Etiology and Clinical Features
Mild extrinsic compression of the axillosubclavian veins
SUPERIOR VENA CAVA FILTER PLACEMENT can be identified in 10% to 50% of the normal population
Patients who cannot tolerate anticoagulation (see Box 3-7) on imaging studies when provocative arm maneuvers are
and have progression of venous thrombosis or clini- performed.64,65 The most common causes for pathologic
cally significant pulmonary embolism are candidates for venous stenosis are prior or existing central venous cath-
filter insertion into the SVC38,58-60 (Fig. 17-14). Details of eters or pacemaker wires, intimal hyperplasia related to
A B
544 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
ipsilateral hemodialysis access, and extrinsic compression Problematic upper extremity vein stenosis occurs most
by musculoskeletal structures66,67 (Box 17-2 and Fig. 17-15). notably in patients with arm hemodialysis grafts or fistu-
Because stenoses develop slowly and the collateral circu- las. About 50% of dialysis patients with prior subclavian
lation often is adequate, many patients tolerate these le- vein catheters develop significant obstructions, which are
sions as long as the vessel does not become completely attributed to direct vein injury, venous turbulence and
occluded. A small percentage of individuals becomes supraphysiologic blood flow, and catheter motion within
symptomatic from the existing stenosis or subsequent the vessel.10,15 Extrinsic compression also can be identified
thrombosis. in a substantial number of dialysis patients without a his-
tory of indwelling catheters.68 The increased flow from
the arm graft or fistula exaggerates the pressure gradient
(and therefore the significance) of even moderate down-
BOX 17-2 stream stenoses. Although these lesions are most com-
mon near the venous anastomosis and at sites of prior
C AU S E S O F U P P E R temporary catheters, they may occur at any place in the
EXTREMITY VENOUS outflow veins.
NARROWING Many patients have arm swelling, pain, and superfi-
cial varicosities. Hemodialysis graft dysfunction is com-
Vascular access devices (prior or existing)
mon, including elevated venous pressures at dialysis,
Extrinsic compression
poor shunt flow, or eventual graft thrombosis.
Musculoskeletal structures
Neoplasm/adenopathy
Intimal hyperplasia Imaging
Outflow veins of dialysis grafts CROSS-SECTIONAL TECHNIQUES
Trauma/surgery
Stenoses of the central upper extremity veins are
Radiation therapy
detected by color Doppler sonography or MR or CT
Vasospasm
venography. However, some patients require catheter ve-
nography prior to endovascular or surgical treatment.
A B
C D
FIGURE 17-15 Extrinsic compression of both subclavian veins from thoracic outlet syndrome. A, Patent left subclavian vein (SCV).
Lucency in the vessel is due to inflow from the unopacified internal jugular vein. B, With arm in abduction, there is mild narrowing of the
left SCV with few collaterals. C, Right SCV in neutral position. D, With arm in abduction, near-complete occlusion of the right SCV is seen
with exuberant filling of collateral channels.
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 545
Provocative maneuvers may be required to uncover the The presence of an extensive collateral network
obstruction.65,69 around a stenosis is an indicator of hemodynamic sig-
nificance. Moderate stenoses can be assessed by mea-
CATHETER VENOGRAPHY suring a focal pressure gradient ("3 to 5 mm Hg) across
Upper extremity venous stenoses usually are smooth the lesion (Fig. 17-19).
and focal (Fig. 17-16). It may be difficult to differentiate
extrinsic compression (caused by musculoskeletal structures
Treatment
or tumor) from intrinsic mural disease (see Fig. 17-15).
Several conditions can mimic fixed obstruction, including ENDOVASCULAR THERAPY
vasospasm from catheter or guidewire manipulation or Balloon angioplasty is the first-line therapy for hemody-
trauma (Fig. 17-17) and external compression from an namically significant venous stenoses. Obstructions can
overlying surgical drape or compression between the be approached directly from an antecubital or upper arm
humerus and ribs in arm adduction (Fig. 17-18). vein, a common femoral vein, or through a dialysis graft,
A B
A B
546 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A B
A B
A B
C
548 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
for central and peripheral lesions.79 Stent restenosis or caused by chronic infection such as histoplasmosis.82
may be relieved with balloon angioplasty, with or The SVC is affected in more than one third of cases;
without placement of additional stents (Fig. 17-22). the pulmonary artery and bronchi also may be involved
Primary assisted patency rates with angioplasty are (see Chapter 14).
excellent in most series. Periodic maintenance of these Significant SVC or bilateral brachiocephalic vein ste-
lesions should be anticipated. Complications of stent nosis or obstruction can lead to the superior vena cava
placement include vein rupture and stent migration, syndrome. This condition is marked by facial and neck
which can be disastrous (Fig. 17-23). swelling, bilateral arm swelling, cyanosis, distention of
superficial veins, shortness of breath, hoarseness, and
SURGICAL THERAPY headache. Left untreated, severe laryngeal edema or ce-
For brachiocephalic vein occlusions, direct bypass with rebral congestion with altered mental status and, even-
prosthetic material or jugular-jugular bypass may tually, coma can ensue. Thus, SVC syndrome may be
be performed. For central subclavian vein occlusions, life-threatening.
internal jugular to subclavian vein transposition is effec-
tive. For peripheral subclavian and axillary venous oc-
Imaging
clusions, direct axillary-jugular bypass is advocated.
Although these operations are feasible, they are rarely CROSS-SECTIONAL TECHNIQUES
ever done. Although sonography cannot directly evaluate the SVC,
alterations in spectral waveform from both subclavian
Superior Vena Cava Obstruction veins (e.g., lack of normal reflected atrial activity and re-
(Online Cases 12 and 39) spiratory phasicity or response to provocative maneu-
vers) should raise suspicion. CT and MR angiography
Etiology and Clinical Features are extremely effective in the diagnosis of SVC obstruc-
Obstruction of the SVC is the result of luminal disease tion.33,83 Findings include intraluminal defects, nonopaci-
(thrombus or tumor), extrinsic compression (tumor or fication of the vessel, extrinsic compression or mass invasion,
adenopathy), or mural disease (intimal hyperplasia or and presence of collateral channels (Fig. 17-24; see also
tumor invasion). The lesion may be stenotic or frankly Fig. 17-8). The latter finding usually is associated with
occlusive. A variety of underlying diseases is respon- symptomatic disease.
sible80,81 (Box 17-3). Bilateral brachiocephalic vein ob-
struction causes almost equivalent hemodynamic dys- CATHETER VENOGRAPHY
function. In older series, infection or malignancy Catheter venography is reserved for cases in which
(particularly lung cancer) were responsible in at least cross-sectional studies are equivocal or transcatheter
90% of cases. However, indwelling vascular devices treatment is being considered. The SVC can be imaged
(e.g., infusion catheters, pacemaker wires) are an in- from one or both antecubital veins, the internal jugular
creasingly common cause of SVC stenosis. vein, or the femoral vein. Stenoses caused by indwell-
Fibrosing mediastinitis is a localized or diffuse infiltra- ing or prior devices usually are long and smooth. Extrin-
tive disease of the mediastinum that may be idiopathic sic masses efface the lumen (see Fig. 17-24). Collateral
A B
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 549
A B
BOX 17-3 vessels fill when contrast is injected above the obstruc-
tion. Associated narrowing of the brachiocephalic (and,
C AU S E S O F S U P E R I O R occasionally, the internal jugular) vein is common.
V E N A C AVA S T E N O S I S O R
OCCLUSION
Treatment
Medical devices MEDICAL THERAPY
Central venous catheters For malignant obstructions with severe SVC syndrome,
Pacemakers urgent chemotherapy and/or radiotherapy is used to
Malignancy treat the underlying cause of disease. Intravenous corti-
Lung cancer costeroids and diuretics also have a role to play. Patients
Mediastinal tumor (e.g., lymphoma, metastases) may notice transient worsening of symptoms with the
Primary leiomyosarcoma onset of radiation therapy as the tumor swells. Antico-
Inflammation agulation is given to limit clot progression.
Fibrosing mediastinitis
Infection (e.g., tuberculosis) ENDOVASCULAR THERAPY
Trauma/surgery Catheter-directed therapy should be considered when
Thrombophilic state medical therapy fails for moderate to severe SVC syn-
Radiation therapy drome, severe arm swelling, or for maintenance of di-
Intimal injury: chemotherapeutic agents alysis access function. Most patients with causative
Aortic or brachiocephalic artery aneurysm malignancy die of their underlying disease; the purpose
of catheter-based treatment is short-term palliation of
550 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
B C D
E F G
FIGURE 17-24 Superior vena cava (SVC) syndrome in a patient with lung cancer. A and B, Computed tomography (CT) scans show
soft tissue in the mediastinum surrounding the central veins with an enlarged azygous arch (arrow) serving as a collateral. C, Coronal
fluorodeoxyglucose positron emission tomography image shows intense uptake in the region of suspected mediastinal disease (arrow)
and elsewhere in the body. D, Central venography shows the extrinsic malignant disease encasing the brachiocephalic vein-SVC confluence.
E, Balloon angioplasty only partially improved flow down the jugular vein. F, Wallstent was inserted into the stenosis, but the stent slipped
forward and is now precariously positioned in the SVC (G).
17. UPPER EXTREMITY VEINS AND SUPERIOR VENA CAVA 551
symptoms. On the other hand, long-term patency is the be repositioned and then reinserted after the stent is
goal in patients with benign SVC obstruction. deployed.91
For benign SVC stenoses, balloon angioplasty is some- For malignant SVC obstructions, stents are virtually
times sufficient. However, some experts maintain that always used92-94 (see Fig. 17-24 and Fig. 17-25). In SVC
stent placement is now the treatment of choice in most syndrome, inline flow from one internal jugular vein is
cases, with durable symptom relief achieved in more than usually sufficient to relieve symptoms. Stents can be
90% of cases.84-89 placed through venous access from above or below the
For benign SVC occlusions and difficult stenoses, stents occlusion. If the obstruction can be traversed only from
are preferable. Thrombolysis precedes angioplasty if above, a snare placed from the femoral vein can be used to
acute or subacute clot is present in the vena cava or cen- capture the guidewire. The procedure is then continued
tral thoracic veins. Otherwise, angioplasty and stent in- from the groin. The stenosis often is predilated with an
sertion may be used alone. Stents may be placed safely angioplasty balloon to ensure it opens and to delineate its
over pacemaker wires.90 Central venous catheters may length. Heparin is given during the procedure.
A B
C D E
FIGURE 17-25 Superior vena cava (SVC) stent placement. A, Computed tomography scan shows soft tissue density in the right
mediastinum encasing the SVC (arrow) due to spread from lung cancer (B). C, Left jugular vein access was used for central venography, which
shows complete SVC occlusion (arrow). D, The occlusion was crossed. With additional right femoral vein access, the occlusion was crossed
again to provide access to the right brachiocephalic vein (arrow). E, Finally, dual kissing stents were deployed across both brachiocephalic
veins into the SVC.
552 IV. PULMONARY VASCULATURE AND VENOUS SYSTEMS
A variety of different devices has been used for this Significant venous trauma that requires specific ther-
purpose, including Wallstents, nitinol stents, Gianturco apy is far less common than arterial injury, and venog-
Z-stent, and Palmaz stents. Large stent, diameters ("16 mm) raphy is rarely indicated. Color Doppler sonography is
are required; stents are purposely oversized to ensure that an excellent tool for screening this population. Unsus-
they remain well secured to the SVC wall after deploy- pected venous trauma often is detected during sur-
ment. If the occlusion involves the confluence of the bra- gery for an associated arterial injury. The injured vein
chiocephalic veins, stents may be extended into one vessel is then treated by direct repair, bypass grafting, or liga-
across the ostium of the other. Alternatively, a Y-shaped tion. Balloon catheter tamponade or stent-graft inser-
stent configuration may be created by laying stents into tion for life-threatening large thoracic vein trauma also
each brachiocephalic vein (see Fig. 17-25). has been described.107-109
Benign SVC obstructions can be relieved in almost
every case, with dramatic and rapid relief of symp-
Neoplasms
toms.84-89 In one large series comparing percutaneous
and open surgical repair, 3-year primary patency rates Almost all tumors that affect the SVC arise from the lung
were essentially identical (44%).84 Still, assisted primary or mediastinum. Primary tumors of the SVC are an un-
patency was much better in stented patients, who also usual cause of SVC syndrome.110,111 Most are leiomyosarco-
had much lower 30-day mortality. mas. The diagnosis is usually made by CT or MR imaging,
For malignant obstructions, partial or complete re- and transvenous biopsy may be performed to confirm the
sponse is observed in 87% to 97% of individuals.86,87,95-98 diagnosis.
Most patients with malignant disease die of the underly-
ing disease with a patent stent. Major complications are
Aneurysms
rare and include early or late stent thrombosis. Immedi-
ate or delayed stent migration is a particular problem Aneurysms of upper extremity and thoracic veins are
when placing SVC stents (see Fig. 17-24). This event can rare.112-114 The most common site is the internal jugular
be catastrophic if cardiac rupture or malignant arrhyth- vein. Congenital jugular vein phlebectasia is another un-
mia ensues. The operator should choose a stent of suffi- usual cause for enlargement of this vessel.115 The diagno-
cient length and avoid laying most of it central to the sis is made by color Doppler sonography. Because of the
stenosis. He or she must be thoroughly familiar with great propensity for thrombus formation and pulmonary
techniques to capture and remove errant stent devices embolism, venous reconstruction is advisable.
(e.g., direct snaring, balloon or guidewire-assisted snar-
ing, or redeployment).99,100
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of malignant obstruction of the superior vena cava. Cardiovasc injuries: case reports. J Trauma 1994;37:111.
Intervent Radiol 2007;30:959. 108. Azizzadeh A, Pham MT, Estrera AL, et al. Endovascular repair of
99. Warren MJ, Sen S, Marcus N. Management of migration of a SVC an iatrogenic superior vena caval injury: a case report. J Vasc Surg
Wallstent into the right atrium. Cardiovasc Intervent Radiol 2008; 2007;46:569.
31:1262. 109. Anaya-Ayala JE, Charlton-Ouw KM, Kaiser CL, et al. Successful
100. Taylor JD, Lehmann ED, Belli AM, et al. Strategies for the man- emergency endovascular treatment for superior vena cava injury.
agement of SVC stent migration into the right atrium. Cardiovasc Ann Vasc Surg 2009;23:139.
Intervent Radiol 2007;30:1003. 110. Spaggiari L, Regnard JF, Nottin R, et al. Leiomyosarcoma of the
101. Smith SL, Manhire AR, Clark DM. Delayed spontaneous superior superior vena cava. Ann Thorac Surg 1996;62:274.
vena cava perforation associated with a SVC Wallstent. Cardiovasc 111. Tovar-Martin E, Tovar-Pardo AE, Marini M, et al. Intraluminal
Intervent Radiol 2001;24:286. leiomyosarcoma of the superior vena cava: a cause of superior
102. Martin M, Baumgartner I, Kolb M, et al. Fatal pericardial tampon- vena cava syndrome. J Cardiovasc Surg (Torino) 1997;38:33.
ade after Wallstent implantation for malignant superior vena 112. Calligaro KD, Ahmad S, Dandora R, et al. Venous aneurysms:
cava syndrome. J Endovasc Ther 2002;9:680. surgical indications and review of the literature. Surgery 1995;
103. Recto MR, Bousamra M, Yeh Jr T. Late superior vena cava perfo- 117:1.
ration and aortic laceration after stenting to treat superior vena 113. Kersting S, Roessel T, Hinterseher I, et al. Isolated aneurysm of
cava syndrome secondary to fibrosing mediastinitis. J Invasive the internal jugular vein. Vasa 2008;37:371.
Cardiol 2002;14:624. 114. Goddziuk K, Czekajska-Chehab E, Wrona A, et al. Saccular aneu-
104. Brown KT, Getrajdman GI. Balloon dilation of the superior vena rysm of the superior vena cava detected by computed tomogra-
cava (SVC) resulting in SVC rupture and pericardial tamponade: a phy and successfully treated with surgery. Ann Thorac Surg 2004;
case report and brief review. Cardiovasc Intervent Radiol 2005;28:372. 78:e94.
105. Moore Jr WM, Hollier LH, Pickett TK. Superior vena cava and 115. Haney JC, Shortell CK, McCann RL, et al. Congenital jugular vein
central venous reconstruction. Surgery 1991;110:35. phlebectasia: a case report and review of the literature. Ann Vasc
106. Kang TL, Dudick C, Ashiku S, et al. Blunt rupture of the subclavian- Surg 2008;22:681.
innominate venous junction: case report and review of literature.
J Trauma 2009;66:1728.
S E C T I O N V
MISCELLANEOUS VASCULAR
INTERVENTIONS
C H A P T E R
18
Vascular Access Placement and
Foreign Body Retrieval
Karim Valji
The demand for long-term central venous catheters are reduced. Although valved catheters require less fre-
(CVCs) has increased dramatically over the past several quent flushing, they actually confer no benefit in terms of
decades. CVCs are used for infusion of drugs (e.g., antibi- catheter dysfunction or vascular thrombosis.4-6 Some
otics, chemotherapeutic agents), administration of blood CVCs have a silver ionimpregnated cuff or silver coating
products, blood sampling, hyperalimentation, and dialy- that is meant to serve as an instant antimicrobial barrier;
sis and apheresis. In the past, CVCs were placed exclu- however, the value of this feature has been challenged.7,8
sively by surgeons in the operating room. Interventional On the other hand, metaanalysis of existing literature
radiologists have now assumed the major role in the inser- supports the value of anti-infective agents incorporated
tion of these devices.1 In some hospitals, vascular access into the inside and outside of the catheter body in reduc-
placement is the most commonly performed procedure in ing device-related bloodstream infections (BSI).9
the interventional radiology suite. Tunneled hemodialysis and apheresis catheters are short,
Image-guided placement of a CVC has several advan- large-bore (typically 13.5 to 14.5 Fr), dual-lumen devices
tages over purely operative insertion.2,3 The risk of capable of handling high flow rates (e.g., 300 to 500 mL/
immediate complications such as pneumothorax, arterial min) (Fig. 18-3). These catheters have staggered or non-
puncture, and catheter malposition is almost completely staggered endholes or split lumens and are manufactured
eliminated. Precise positioning of the catheter tip is in preset lengths. From the right internal jugular (IJ) vein,
almost guaranteed. Finally, imaging is critical when placing 19- to 23-cm tip-to-cuff devices are usually appropriate.
catheters through occluded thoracic or neck veins or out- From the left IJ, 23- to 28-cm devices are often necessary.
side the chest (e.g., into the inferior vena cava [IVC]). Tunneled hemodialysis catheters must be distinguished
from nontunneled temporary catheters (usually placed by
nephrologists) intended for several sessions of acute,
ACCESS PLANNING emergent dialysis. No single catheter type has been proven
to be most effective. Still, there is some evidence that split
and symmetric tip catheters (e.g., Palindrome type) have a
Devices longer functional lifespan than the traditional staggered
Tunneled, cuffed external infusion catheters are made of sili- tip devices.10-14 In principle, separation of the uptake and
cone or polyurethane-based material. They are manufac- return lumens is necessary to prevent recirculation, which
tured with one, two, or three lumens in diameters from can significantly diminish the efficiency of dialysis.15 Even
3 to 12.5 French (Fr) (Fig. 18-1). These devices are inserted so, the symmetrically tipped Palindrome catheter is re-
into a large vein and then travel through a subcutaneous ported to achieve the lowest recirculation rates among the
tunnel before exiting the skin. A Dacron cuff embedded various catheter models that are available.14
on the shaft incites a fibrotic reaction that ultimately Implantable ports are constructed from a variety of
secures the catheter in place and impedes the spread of materials, including titanium and plastic (Fig. 18-4). A
infection from the skin exit site to the circulation. Infusion silicone or polyurethane catheter is connected to a reser-
catheters have endholes or side valves (e.g., Groshong voir with a silicon window that is accessed through the
type). The valve design is intended to allow fluid injection skin using a noncoring (Huber) needle. The entire sys-
and (possibly) blood aspiration but prevent blood or air tem is buried in the subcutaneous tissue of the chest or
from entering the catheter when it is not in use (Fig. 18-2). arm (or even the thigh or abdomen). These devices are
In theory, the risks of catheter occlusion and air embolism available in single- and double-lumen configurations.
559
560 V. MISCELLANEOUS VASCULAR INTERVENTIONS
Device Selection
FIGURE 18-3 Hemodialysis catheters. Top, 13.5-Fr catheter with
staggered lumens (proximal endhole is the arterial lumen). (Courtesy The selection of the most appropriate catheter in an
of Bard Access Systems, Salt Lake City, Utah.) Bottom, Split dialysis individual case should be made jointly by the referring
catheter. (Courtesy of Medcomp, Harleysville, Pa.) physician, interventionalist, and patient. Several factors
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 561
TABLE 18-1 Guidelines for Access Device Selection common femoral vein. Practically, this situation occurs
in patients requiring long-term hemodialysis. However,
Device Purpose or Situation
thrombotic, stenotic, and infectious complications are
External, tunneled catheter Continuous use greatest with tunneled femoral catheters, which are
Multiple, simultaneous uses prone to dysfunction and retraction 23-25 As a last resort,
Patient preference
Implantable port Intermittent use
central venous access is obtained directly into the IVC
Immunocompromised patient through a translumbar or transhepatic approach.26-28
Patient preference
High-flow tunneled catheter Hemodialysis
Apheresis Patient Preparation
PICC Short-term use (!23 mo)
Infrequent blood drawing
With the notable exception of PICCs, vascular access
(lifetime risk for dialysis is low) insertion in an interventional suite demands the same
aseptic environment as is found in an operating room.
PICC, peripherally inserted central catheter.
All procedures begin with antibacterial cleaning of sur-
faces that may come in contact with the patient, wide
surgical preparation of the operating field, surgical
are considered, including intended purpose, frequency scrub by all operators, and maintenance of strict sterile
and duration of use, underlying risk factors for infection technique during the case. Some interventionalists
or venous thrombosis, and patient preference for an give prophylactic antibiotics (e.g., 1 g of cephazolin IV)
external or implanted device (Table 18-1). Tunneled in- within 1 hour of placement of tunneled catheters or
fusion catheters and implantable ports are only appro- ports, even though the benefit of this step is question-
priate when the anticipated duration of need for con- able. Bacteremia or sepsis is a contraindication to place-
tinuous or periodic vascular access is more than several ment of tunneled catheters and implantable ports.29
weeks. Whereas the risk of device-related infections is Coagulation parameters should be checked and cor-
probably lower with chest ports, the consequences of rected before the procedure (see Chapter 2). One recent
infectious and other port site complications are more study suggested that the standard coagulation thresh-
problematic. Finally, it is wise for the operator to person- olds for vascular interventional procedures may be
ally confirm the device request just before placement to relaxed with tunneled CVC placement (e.g., acceptable
avoid an egregious implantation error due to miscom- with platelet count greater than 25,000/mm3 or interna-
munication or an acute change in patients condition. tional normalized ratio less than 2.0).30
A B
FIGURE 18-7 Pinch-off syndrome. A, Surgically placed right subclavian vein port. B, Some months later, port was no longer functional. Chest
radiograph shows catheter fracture at site of pinch off in the costoclavicular space (long arrow). The distal catheter fragment has embolized to
the left pulmonary artery (short arrow).
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 563
C D
E F G
FIGURE 18-7, contd C, From a femoral vein approach, an Omniflush catheter has been advanced into the left pulmonary artery. D, The
catheter was exchanged for the guiding catheter and gooseneck snare. E, The upper free end of the catheter fragment was snared with the retrieval
device. The fragment was then pulled out of the heart (F) and into the large-caliber vascular sheath (G) for removal from the body.
564 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B
C
FIGURE 18-8 Axillary vein entry. A, Sagittal sonogram shows the relationship between the artery (a) and vein (v). B, Longitudinal image
of the axillary-subclavian artery with a side branch (arrow). C, Longitudinal image of the axillary vein. D, Micropuncture needle is inserted
under sonographic guidance with constant aspiration on the saline-filled tubing and syringe.
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 565
A B C
FIGURE 18-9 Inferior vena cava (IVC) vascular access placement. A, A guidewire is being placed in the IVC from the right common
femoral vein through a diseased iliac system. B, With the patient prone, a 20-gauge, 15-cm Chiba needle is directed toward the guidewire
from the right flank. C, The 55-cm tip to cuff dialysis catheter is in place with the tip near the cavoatrial junction.
use the laterally located femoral artery pulse as a land- Transhepatic venous access is necessary for individuals
mark. Catheters are tunneled laterally onto the thigh or whose only patent central vein is the suprarenal IVC.
lower abdomen (see later discussion). Even though this route is feasible in most cases, long-
IVC puncture may be required if all potential access term catheter function is a serious problem.26,28 Finally,
sites in the chest, arms, and groin are exhausted.22,27,28,35 transrenal venous entry into the IVC has been described
Prior CT scans are reviewed to identify any obstacles or for patients with end-stage renal disease who require
contraindications to the intended route. Initially, a tunneled dialysis catheters.36
sheath, guidewire, or catheter may be placed into the
IVC from the groin, although this step is not mandatory
(Fig. 18-9). Bony landmarks alone may be used for caval
Catheter Tip Position (Video 18-3)
entry. The patient is then placed prone on the interven- The manufacturers of most vascular access devices in-
tional table. A skin site is chosen on the right flank above struct the operator to place the catheter tip in the SVC or
the iliac crest just lateral to the vertebral column. It is at the cavoatrial junction. However, the long-term fail-
critical to plan a cephalic track into the IVC to avoid a ure rate of CVCs placed with the tip at these locations at
sharp right angle turn as the needle enters the vessel, the termination of the procedure is significant. Most
which can make sheath and catheter insertion exceed- CVCs migrate 3 to 4 cm upward from the supine to
ingly difficult. A long, 18- to 20-gauge needle is then ad- standing position; PICCs move about 2 cm caudally
vanced toward the catheter/wire in the IVC or toward when the arm is adducted after placement.37-39 Although
the right lateral aspect of the spine in the calculated not widely understood nor even accepted outside the
position of the IVC from prior imaging studies. Biplane interventional radiology community, it is now standard of
fluoroscopy or frequent tube angulation is necessary to practice to position the catheter tip in the upper to mid-right
avoid overshooting the vena cava. Once blood is aspi- atrium with the patient supine.40,41 At this location, the
rated and contrast injection confirms the location, the catheter endholes will rarely become obstructed by a fibrin
remainder of the procedure is similar to catheter place- sheath because the tip hangs freely in the right atrium
ment from other access routes. A stiff guidewire is neces- rather than plastered against the caval wall (Fig. 18-10).
sary for placement of the peel-away sheath. Several nonrandomized clinical studies lend credence to
566 V. MISCELLANEOUS VASCULAR INTERVENTIONS
as it makes a turn out of the vein and toward the chest. incision. The venotomy may be closed with Dermabond,
For catheters with staggered lumens, the arterial lumen Steri-Strips, or suture material.
(proximal port) is positioned with the endhole away Arm ports are inserted above the elbow in a similar
from the right atrial wall for optimal function. The cath- fashion. The tunnel can be very short, allowing the cath-
eter tip should be readjusted if rapid aspiration of blood eter to be pulled from the skin incision to the venotomy
is not possible after placement. Some dialysis units site using forceps rather than a tunneling device. Care
prefer to fill catheters with high-dose heparin (1000 or must be taken to avoid damaging the brachial artery
5000 units/mL) to prevent thrombosis. Others opt for during placement.
citrate solution to avoid the possibility of inadvertent
injection of the anticoagulant. Peripherally Inserted Central Catheters
(Video 18-6)
Implantable Ports (Video 18-5) PICCs are suitable for patients who need short-term cen-
Ports may be placed in the chest or arm (or even the tral vascular access (typically for antibiotics, chemother-
thigh), depending on the patients lifestyle and prefer- apy, or hyperalimentation for up to 4 to 6 weeks).56-59
ence.50-54 Chest ports are easiest to access. The intended However, PICCs must be strictly avoided in patients ex-
port site must have enough subcutaneous fat to accom- pected to require hemodialysis in the future lest potential
modate the device easily and avoid wound dehiscence or access sites become obliterated. It is more cost-effective
skin breakdown. Of note, port incision dehiscence is also for PICCs to be placed at the bedside by specially trained
a concern in patients who have received bevacizumab nurses than by physicians in the IR suite.60 However, tip
therapy within 10 days of insertion.55 However, a port malposition is more frequent (about 10%) without fluoro-
can be difficult to access if there is too much surrounding scopic guidance.61 Radiologic placement is indicated
adipose tissue or if it is poorly supported by underlying when bedside insertion is unsuccessful or unavailable.
bone. Ideally, the port septum should be about 0.5 to The dilator or sheath is inserted into the accessed vein.
2 cm below the skin surface. The operator should avoid The catheter is cut to size and inserted through the peel-
placement in breast tissue or the axilla. away sheath with the accompanying stylet to assist with
After venous access is obtained (see earlier discus- catheter passage. It is then advanced into the upper right
sion), a 3- to 5-cm transverse incision is made on the atrium and flushed with heparin lock solution. The hub
anterior chest wall using a No. 10 or 15 blade after infil- is secured to the skin with suture material or an adhesive
tration with 1% or 2% lidocaine with epinephrine. appliance.
Bleeding from small arterial branches always stops with
manual compression or brief occlusion with a small
hemostat. A pocket is created inferior to the incision us- ACCESS MANAGEMENT
ing sharp and blunt dissection. The pocket should be
large enough to accommodate the port and allow easy
Catheter and Exit Site Care (Video 18-7)
closure of the wound. Some interventionalists (but not
most) place two stay sutures from eyelets in the port Meticulous catheter and exit site care is the key to limiting
base through the anterior fascial plane to secure it in CVC-related infectious complications. Patient or care-
place after insertion into the pocket.54 giver education is done before and after device placement
The catheter is tunneled through the subcutaneous by a specially trained nurse. Protocols for catheter and
track and then connected securely to the port hub, usu- wound care and for catheter flushing vary somewhat
ally with a retention sleeve. The port is placed in the among institutions. A sterile gauze or occlusive plastic
pocket well below the incision. At the neck, the catheter dressing is kept over the fresh incision or exit site; in trials
is cut to size based on measured intravascular length (see of dialysis catheters, rates of exit site and BSI are similar
earlier) and then inserted into the vein using a peel-away for both coverings.62 The incision must be kept com-
sheath. The catheter tip should land in the upper to mid pletely dry for at least 3 days. Various sorts of topical
right atrium. Under fluoroscopy, the entire course of the antiinfectives are also popular. For dialysis catheters, mu-
catheter is examined for kinks. The device is accessed pirocin (and possibly Neosporin or povidone-iodine)
with a noncoring (Huber) needle and flushed with hepa- ointment may reduce catheter-related infections.62
rin lock solution (100 units/mL). The incision may be The exit site, incision, and tunnel track are examined
closed with interrupted absorbable sutures in the sub- daily by the patient or caregiver for signs of infection,
cutaneous layer to approximate tissues and continuous catheter withdrawal, catheter fracture, wound dehiscence,
absorbable suture in the subcuticular layer. Some or skin breakdown. The site also should be examined by a
operators favor closure with Dermabond skin adhesive. physician or nurse within 5 to 7 days of placement. By
Steri-Strips and a sterile dressing are placed over the tradition, CVCs are flushed with heparin solution weekly
568 V. MISCELLANEOUS VASCULAR INTERVENTIONS
and after each use to maintain patency. Some dialysis cen- tical manner to port placement. If there is any evidence
ters prefer trisodium citrate solution for its antimicrobial of actual pocket or tunnel infection, the wound is
and anticoagulant activity.63 Groshong catheters may be packed with iodoform gauze and allowed to heal by
filled with saline and require less frequent flushing. In secondary intention.
randomized trials, the use of antimicrobial catheter lock
significantly diminishes the incidence of BSIs.64,65
COMPLICATIONS
Device Removal (Video 18-8)
Immediate Complications
To remove tunneled catheters, the exit site is sterilized
and the tunnel track anesthetized. In many cases, firm The overall adverse event rate for CVC placement is
steady traction will release the entire catheter. Retention about 4% to 7%.29,53,58,67,68 Immediate complications occur
of the polyester cuff is not associated with an increased less frequently with image-guided placement than with-
risk of subsequent infection.66 Otherwise, blunt and out2,49-54,69 (Table 18-2 and Fig. 18-11). With the exception
sharp dissection are used to separate the device from the of venous thrombosis, procedure-related complication
subcutaneous tissues. If the cuff is far from the skin exit rates generally are lower for PICCs and peripheral ports
site, it is sometimes necessary to perform a cutdown than for devices placed in the chest or neck. However,
over the cuff to release the catheter. The smaller caliber median nerve injury is a remote risk unique to catheter
infusion catheters may fracture if excessive force is ap- insertions in arm veins.70
plied to remove them. If the catheter breaks, it may be
possible to extricate the buried segment with a forceps
under fluoroscopy. Otherwise, intravascular retrieval
TABLE 18-2 Early Complications from Image-Guided
will be necessary (see later discussion). Vascular Access Placement
To remove implanted ports, an incision is made over
the original scar after local anesthesia is applied. Using Event Frequency (%)
sharp and blunt dissection, the port and catheter hub Pneumothorax 0-1
are separated from the surrounding tissue. The fibrous Arterial puncture 1-2
capsule around the port is incised with a dissecting Hemorrhage or hematoma 0-2
scissors or scalpel to release the device. The stay su- Air embolism 1
Catheter malposition 0
tures (if present) are cut, and the port and attached
Venous perforation !1
catheter are removed. The incision is closed in an iden-
A B
FIGURE 18-11 Superior vena cava (SVC) rupture during hemodialysis catheter placement. A, Contrast injection shows extravasation
outside the SVC. B, Several large stainless-steel coils were used to close the leak. Subsequently, a tunneled catheter was placed into the SVC.
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 569
Air embolism can occur during the interval between TABLE 18-3 Late Complications from Image-Guided
removing the dilator and peeling away the sheath. If Vascular Access Placement
this untoward event is suspected, the chest is immedi- Event Frequency (%)
ately examined with fluoroscopy. Conventional teach-
ing recommends placing the patient in the left lateral Catheter occlusion 1-10
Catheter or device migration 0-3
decubitus position to keep the air in the right heart Catheter dislodgment 2-9
chambers and prevent air lock. In reality, the air Catheter fracture 1-9 (PICC)
bolus almost always has already traveled to the pulmo- Wound dehiscence 1
nary artery by the time the embolism is recognized. Port inversion !1
Supplemental oxygen and IV fluids are given, and Central venous thrombosis 0-10 (0.1-0.3/1000 catheter days)
Peripheral vein thrombosis 1-38
the patient is carefully monitored. Air embolism is al- (PICCs)
most always self-limited, but fatal events have been Local infection 1-7
reported.71 Catheter-related bacteremia 1-4
Persistent blood oozing from the skin exit site is an Bloodstream infections (BSI)
occasional problem. Prolonged manual pressure usually PICCs 2.1/1000 catheter days
Tunneled infusion catheters 1.6/1000 catheter days
resolves the bleeding. Coagulation parameters should
Tunneled dialysis catheters 3/1000 catheter days
be checked and corrected if necessary. In patients Implanted ports 0.1/1000 catheter days
with renal failure, normal hemostasis may be affected
by platelet dysfunction. If necessary, Gelfoam pledgets
or collagen sealant inserted into the tunnel may be help-
ful. Silver nitrate can be applied (to the subcutaneous
tissue only) to achieve hemostasis. Some practitioners
favor temporary placement of a purse-string suture at BOX 18-1
the site.72
INFECTIOUS
Fatalities during vascular access placement have been
C O M P L I C AT I O N S
reported from laceration of the central veins or heart by
OF CENTRAL VENOUS
the tip of the dilator or guidewire.73 This catastrophe is
C AT H E T E R S
avoided by advancing the sheath or dilator with careful
fluoroscopic monitoring.
Bacteremia (bloodstream infections, BSI)
Exit site infection
Late Complications Port pocket infection
Subcutaneous tunnel infection
The primary late complications of CVC placement are
Septic thrombophlebitis
infection, catheter occlusion or malfunction, venous
Osteomyelitis
thrombosis, and catheter migration* (Table 18-3).
Endocarditis
Overall, the frequency of infections and catheter-
Septic shock
related thrombosis is substantially higher for tunneled
hemodialysis catheters than for small-bore infusion
catheters.
source.78,79 Initial treatment involves broad-spectrum IV count and negative blood cultures, and have received at
antibiotics or antibiotic lock and local wound care. Skin least 2 days of IV antibiotic therapy.
and blood cultures are obtained to guide ongoing antibi-
otic therapy. If the patient responds to treatment, the de- Catheter Malfunction (Video 18-9)
vice is left in place or exchanged over a guidewire for a Catheter malfunction is a vexing problem in patients
new catheter (see later discussion). Catheter removal is with central venous access devices. The best approach
necessary if these measures fail or if one of the following is prevention: position the catheter tip in the upper or
conditions exist: mid right atrium. Malfunction can occur for several
reasons:
Tunnel infections, port pocket infections, septic
thrombophlebitis, osteomyelitis, or endocarditis79 Fibrin sleeve or clot occluding the endhole
Unstable condition or sepsis Catheter malposition or migration
Isolation of certain microorganisms77 listed in Catheter kinks
Box 18-2 Catheter tip abutting or eroding into the vessel
Markedly compromised immune system wall
Catheter fracture
Even though it is accepted practice to culture
the catheter tip upon retrieval, the impact of this Material obstruction of the catheter endholes occurs
step on patient management is questionable.80 After by two mechanisms. A clot may form at the catheter tip.
removing an infected port, the pocket is irrigated and More commonly, however, a slick fibrin sheath com-
packed with iodoform gauze. The packing is changed posed of fibrin, albumin, lipoproteins, and coagulation
every few days and the wound allowed to heal by sec- factors covers the structure within hours after place-
ondary intention. ment and continues to accumulate over 5 to 7 days.63 If
The timing for reinsertion of a new tunneled catheter bacteria colonize this surface, a biofilm is produced
in a patient with catheter-related BSI is very controver- through which antimicrobial agents are relatively resis-
sial.77 Ideally, the interventionalist should wait until the tant. If the catheter tip apposes a vein wall, this coating
entire course of antibiotics has been given, but such matures into a dense sleeve including collagen and
delay is often impractical. At the very least, the patient smooth muscles cells. The sleeve can eventually ob-
should become afebrile, have a normal white blood cell struct the catheter endhole81 (Fig. 18-12). Fluid usually
BOX 18-2
O R G A N I S M S T H AT
G E N E R A L LY R E Q U I R E
CENTRAL VENOUS
C A T H E T E R R E M O VA L
Staphylococcus aureus
Acinetobacter baumannii
Agrobacterium species
Aspergillus species
Bacillus species
Candida species
Corynebacterium jeikeium
Malassezia furfur
Mycobacterium species
Pseudomonas aeruginosa
Other Pseudomonas species
Stenotrophomonas species
Other gram-negative rods FIGURE 18-12 Fibrin sheath. Contrast injected through the
catheter lumen runs back along the catheter shaft (arrow) rather than
exiting the catheter freely.
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 571
A B C
FIGURE 18-15 Spontaneous displacement of right chest port catheter. A, Chest radiograph shows that the right internal jugular vein
catheter has migrated back into the right subclavian vein. B, Through a long vascular sheath placed in the right femoral vein, a pigtail type
catheter and guidewire are used to loop the port catheter. Withdrawal of the pigtail catheter allowed the port catheter to prolapse back
down the superior vena cava into proper position (C).
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 573
INTRAVASCULAR FOREIGN BODY the trilobed En Snare (Merit Medical).111 The former
RETRIEVAL (ONLINE CASE 26) system (Fig. 18-16) is available in a wide range of loop
diameters and catheter sizes (standard, 5 to 35 mm, 4 to
6 Fr; micro, 2 to 7 mm, 3 Fr). The latter system (Fig. 18-17)
Sources is made in both standard (6 to 45 mm, 6 to 7 Fr) and
A wide variety of objects can become lodged in the vascu- mini sizes (2 to 8 mm, 3.2 Fr). An 8- to 10-Fr (or larger)
lar system, including catheter and guidewire fragments, vascular sheath is inserted in the common femoral or
coils and Amplatzer occluding devices, stents, balloon internal jugular vein. The sheath should be large enough
fragments, IVC filters or fragments, and bullets.106-108 The to accommodate the collapsed foreign body and snare
ultimate destination of a foreign body depends on its to minimize trauma to the access vein as the object is
shape, size, and stiffness, and on the hemodynamics of removed.
the local circulation. In some cases, catheter fracture (e.g., The guiding catheter provided with the kit is ad-
from pinch-off syndrome) is detected days to years after vanced through the vascular sheath up to the foreign
the actual event (see Fig. 18-7). Guidewires may become body; the snare is inserted and exposed, and then
entrapped within IVC filters, usually during blind central manipulated around a free end (or loop) of the fragment
venous catheter insertion into a neck or chest vein. (Fig. 18-18; see also Fig. 18-7). Often, both ends of the
Potential complications of intravascular foreign bod- fragment abut the vein wall. In this case, the midsection
ies include clot formation and embolization, sepsis, car- of the fragment is engaged with a pigtail (or other) cath-
diac dysrhythmias, and vascular or heart perforation eter. The pigtail is withdrawn at the access site to reposi-
with ensuing hemorrhage or cardiac tamponade. When tion the fragment and free one of the ends. After the
feasible, intravascular foreign bodies should be retrieved fragment is snared (preferably near the tip), the wire loop
by percutaneous means to prevent untoward conse- is cinched around it tightly by withdrawing the snare
quences.109 In most cases, long device dwell time itself is wire while holding the guiding catheter stationary. The
not a reason to avoid attempting removal.110 object then is pulled through the IVC or SVC into the
sheath and out of the body. A loop-snare technique is
also effective when simpler maneuvers do not work (see
Technique Fig. 16-24). Alternatively, an endomyocardial biopsy for-
Several devices are available for endovascular retrieval. ceps device (Ceres Medical Systems) is used to directly
However, the most popular and versatile devices are grab the fragment without the need for a free end. Larger
the Amplatz nitinol gooseneck snare (Microvena) and foreign bodies (e.g., IVC filters, stents) may require more
FIGURE 18-16 Amplatz nitinol gooseneck snare (Microvena, FIGURE 18-17 EnSnare trilobed retrieval device. (Courtesy of
White Bear Lake, Minn.) with outer 6-Fr guiding catheter. Merit Medical.)
574 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B
C
FIGURE 18-18 Guidewire fragment retrieval. A, A long segment of guidewire was severed during attempted blind placement of a central
venous access device. The wire became lodged in the inferior vena cava. B, A nitinol gooseneck snare was inserted from the left femoral vein
and used to grab the free end of the guidewire. C, The guidewire and snare are removed through a femoral vein sheath.
complex and creative maneuvers for removal107,111-113 femoral vein to capture the end of the wire and dislodge
(Figs. 18-19 and 18-20). In some instances, the device it from the filter.
must be withdrawn into the common femoral or internal
jugular vein and removed through a simple surgical cut-
down.
Results and Complications
There are several ways to approach guidewires that Percutaneous retrieval of catheter and guidewire frag-
have become trapped within IVC filters.114,115 If the ments is successful in greater than 95% of attempts.106,110
guidewire is still exiting the skin, a sheath may be In many cases, even large devices such as intravascular
placed over the wire and advanced into the IVC (Fig. stents and IVC filters can be removed safely.116 One re-
18-21). Gentle pressure may allow the wire to become view of IVC filter removals (mostly from the heart) cal-
dislodged from the catheter, both of which are then re- culated a 69% success rate.116,117 The overall mortality
moved. Otherwise, a loop snare is introduced from the rate from all attempts was 6%.
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 575
A B
C
FIGURE 18-19 Retrieval of a Palmaz stent. A, Stent has slipped off an angioplasty balloon during renal artery treatment. B, A nitinol snare
was placed around the lower end of the collapsed stent after the angioplasty balloon was removed. C, The stent was pulled into an 8-Fr sheath
and removed.
576 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B C
D E
FIGURE 18-20 Retrieval of unstable Wallstent. Following orthotopic liver transplantation, hepatic confluence and inferior vena cava
(IVC) stenosis had prompted placement of single IVC and dual hepatic vein Wallstents in Y-configuration. A, At the time of routine
transjugular liver biopsy several months later, the central hepatic vein stent was noted to have migrated into the IVC (arrow). B, From the
right jugular vein, a wire and then angled catheter were advanced through the barrel of the malpositioned stent. Manipulations caused the
stent to move caudally. Through a 12-Fr vascular sheath, a gooseneck snare was advanced alongside the stent. C, The end of the guidewire
running through the stent was captured with the snare. D, Both wires exiting the sheath at the neck were pulled, causing the stent to collapse
and then be pulled into the sheath (E).
18. VASCULAR ACCESS PLACEMENT AND FOREIGN BODY RETRIEVAL 577
A B
C D
FIGURE 18-21 Inferior vena cava (IVC) guidewire entrapment. A, During bedside placement of a central venous line, the house officer
felt resistance upon guidewire withdrawal from the subclavian vein. Subsequent image at fluoroscopy shows guidewire trapped in the legs of
a Greenfield filter. B, A 5-Fr catheter was advanced over the wire into the IVC. C, A long vascular sheath was introduced over the catheter for
stability. D, After advancing the entire system down off the filter neck, the guidewire was dislodged and ultimately removed.
578 V. MISCELLANEOUS VASCULAR INTERVENTIONS
90. Janne dOthee B, Tham JC, Sheiman RG. Restoration of patency 103. Walshe C, Phelan D, Bourke J, et al. Vascular erosion by central
in failing tunneled hemodialysis catheters: a comparison of venous catheters used for total parenteral nutrition. Intensive Care
catheter exchange, exchange and balloon disruption of the fi- Med 2007;33:534.
brin sheath, and femoral stripping. J Vasc Interv Radiol 2006; 104. Bessoud B, de Baere T, Kuoch V, et al. Experience at a single insti-
17:1011. tution with endovascular treatment of mechanical complications
91. National Kidney Foundation. K/DOQI clinical practice guide- caused by implanted central venous access devices in pediatric
lines for vascular access, 2006. Am J Kidney Dis 2006;48:S248. and adult patients. AJR Am J Roentgenol 2003;180:527.
92. Allen AW, Megargell JL, Brown DB, et al. Venous thrombosis associ- 105. Collares FB, Faintuch S, Kim SK, et al. Reinsertion of accidentally
ated with the placement of peripherally inserted central catheters. dislodged catheters through the original track: what is the likeli-
J Vasc Interv Radiol 2000;11:1309. hood of success? J Vasc Interv Radiol 2010;21:861.
93. Kuriakose P, Colon-Otero G, Paz-Fumagalli R. Risk of deep venous 106. Egglin TK, Dickey KW, Rosenblatt M, Pollak JS. Retrieval of intra-
thrombosis associated with chest versus arm central venous subcu- vascular foreign bodies: experience in 32 cases. AJR Am J Roentgenol
taneous port catheters: a 5-year single-institution retrospective 1995;164:1259.
study. J Vasc Interv Radiol 2002;13:179. 107. Kuo WT, Loh CT, Sze DY. Emergency retrieval of a G2 filter after
94. Cortelezzi A, Moia M, Falanga A, et al. Incidence of thrombotic com- complete migration into the right ventricle. J Vasc Interv Radiol
plications in patients with haematological malignancies with central 2007;18:1177.
venous catheters: a prospective, multicentre study. Br J Haematol 2005; 108. Keele KL, Gilbert PM, Aquisto TM, et al. Bullet embolus to the
129:811. thoracic aorta with successful endovascular snare retrieval. J Vasc
95. Streiff MB. Diagnosis and initial treatment of venous thromboem- Interv Radiol 2010;21:157.
bolism in patients with cancer. J Clin Oncol 2009;27:4889. 109. Tateishi M, Tomizawa Y. Intravascular foreign bodies: danger of
96. Klerk CP, Smorenburg SM, Buller HR. Thrombosis prophylaxis in unretrieved fragmented medical devices. J Artif Organs 2009;12:80.
patient populations with a central venous catheter: a systematic 110. Wang PC, Liang HL, Wu TH, et al. Percutaneous retrieval of dis-
review. Arch Intern Med 2003;163:1913. lodged central venous port catheter: experience of 25 patients in a
97. Agnelli G, Verso M. Therapy insight: venous-catheter-related single institute. Acta Radiol 2009;50:15.
thrombosis in cancer patients. Nature Clin Pract 2006;3:214. 111. Gabelmann A, Kramer S, Gorich J. Percutaneous retrieval of lost
98. Karthaus M, Kretzschmar A, Kroning H, et al. Dalteparin for or misplaced intravascular objects. AJR Am J Roentgenol 2001;
prevention of catheter-related complications in cancer patients 176:1509.
with central venous catheters: final results of a double-blind, 112. Taneja M, Rajan DK. Percutaneous removal of migrated nitinol
placebo-controlled phase III trial. Ann Oncol 2005;17:289. stents from the right ventricle. J Vasc Interv Radiol 2006;17:1213.
99. Verso M, Agnelli G, Bertoglio S, et al. Enoxaparin for the prevention 113. Bochenek KM, Aruny JE, Tal MG. Right atrial migration and per-
of venous thromboembolism associated with central venous cath- cutaneous retrieval of a Guenther Tulip inferior vena cava filter.
eters: a double-blind, placebo-controlled, randomized study in J Vasc Interv Radiol 2003;14:1207.
cancer patients. J Clin Oncol 2005;23:4057. 114. Loehr SP, Hamilton C, Dyer R. Retrieval of entrapped guide wire
100. Couban S, Goodyear M, Burnell M, et al. Randomized, placebo- in an IVC filter facilitated with use of a myocardial biopsy forceps
controlled study of low-dose warfarin for the prevention of cen- and snare device. J Vasc Interv Radiol 2001;12:1116.
tral venous catheter-associated thrombosis in patients with cancer. 115. Duong MH, Jensen WA, Kirsch CM, et al. An unusual complica-
J Clin Oncol 2005;23:4063. tion during central venous catheter placement. J Clin Anesth
101. Mokrzycki MH, Jean-Jerome K, Rush H, et al. A randomized trial 2001;13:131.
of minidose warfarin for the prevention of late malfunction 116. Mitchell WB, Bonn J. Percutaneous retrieval of a Greenfield filter
in tunneled, cuffed hemodialysis catheters. Kidney Int 2001; after migration to the left pulmonary artery. J Vasc Interv Radiol
59:1935. 2005;16:1013.
102. Traynor JP, Walbaum D, Woo YM, et al. Low dose warfarin fails 117. Owens CA, Bui JT, Knuttinen MG, et al. Endovascular retrieval of
to prolong survival of dual lumen venous dialysis catheters. intracardiac inferior vena cava filters: a review of published tech-
Nephrol Dial Transplant 2001;16:645. niques. J Vasc Interv Radiol 2009;20:1418.
C H A P T E R
19
Hemodialysis Access
Erik Ray, Anne C. Roberts
ACCESS CONSTRUCTION tion even these high-risk patients may be suitable for a
fistula.3 The reported failure rates range from 10% to
The ideal hemodialysis access is an endogenous fistula 65%, but the usual figure in modern practice is about
created by surgical anastomosis of an artery and vein. The 15% to 25%.3-8
updated National Kidney Foundation Kidney Dialysis Because a fistula requires 3 to 4 months to mature, it
Outcomes Quality Initiative (NKF-KDOQI) and clinical should be created well in advance of the anticipated need
practice guidelines have set a goal of primary arteriove- for dialysis.1,9 The veins in the arm must not have been
nous fistula construction in at least 65% of all new patients damaged by previous venipunctures. Fistulas are ready
with kidney failure, with ultimately 65% of hemodialysis for use when the blood flow is greater than 600 mL/min,
patients having a native fistula.1 Arteriovenous (AV) vein diameter is at least 0.6 cm, depth under skin is less
accesses are placed as far distally in the upper extremity as than 0.6 cm, and there are discernible vein margins under
possible to preserve proximal sites for future access. Ideal the skin.1 In one postoperative study, fistulas with a diam-
access is within the upper extremity and preferentially eter of at least 4 mm and a blood flow greater than 500
within the nondominant arm if opportunities exist. mL/min had a 95% likelihood of success for dialysis.10 If
an endogenous fistula can be constructed and matures
The radiocephalic (Brescia-Cimino) fistula is a
properly, it should have excellent long-term patency.
side-to-side anastomosis of the radial artery and
A synthetic graft is the alternative to an endogenous
the cephalic vein at the wrist (Figs. 19-1 and 19-2);
fistula. These grafts are commonly made of polytetrafluo-
it is the first choice for a permanent access.1
roethylene (PTFE). They may be placed in the forearm in
A brachiocephalic fistula also can be constructed
a straight configuration from the radial artery to a brachial
between the brachial artery and the cephalic vein1
vein, but a looped configuration from the brachial artery to
(see Fig. 19-1). This access is more likely to result
a brachial vein (Fig. 19-3) usually is preferred.1 Grafts also
in arm swelling or distal ischemia than a more
may be constructed in the upper arm, usually in a looped
peripheral fistula.
configuration from the brachial or axillary artery to a high
The transposed brachiobasilic fistula involves lateral
arm vein. If all possible sites in the arm and chest are
rotation and superficialization of the basilic vein
exhausted, a loop graft can be placed in the thigh from the
to allow easy cannulation (see Fig. 19-1).
common femoral artery to the common femoral vein.
Less common forms include connections between
PTFE grafts may be used much earlier than native
the brachial artery and a median antecubital vein
fistulas, usually within 14 days of placement.1 How-
(brachiomedian antecubital fistula), and between the
ever, they do not have the longevity that can be
femoral artery and saphenous vein.2
achieved with an endogenous fistula. Primary patency
Although an autologous arteriovenous fistula (AVF) rate at 1 year is reported to be approximately 40%.4,11
is the ideal hemodialysis access, it may be difficult or Secondary patency rate ranges from 60% to 90%.1,12
impossible to create successfully in a significant num- The most common reason for failure is development of
ber of patients. Failures are particularly common in a stenosis in the outflow vein, leading to thrombosis of
older and diabetic patients. Still, with careful evalua- the graft.1
581
582 V. MISCELLANEOUS VASCULAR INTERVENTIONS
AVF anastomosis
A B C
FIGURE 19-1 Hemodialysis access. A, Endogenous radiocephalic arteriovenous fistula. Note the inflow radial artery (arrow), arteriovenous
anastomosis (arrowhead), and outflow cephalic vein (curved arrow). B, Endogenous brachiocephalic fistula. Note the inflow brachial artery
(arrow), arteriovenous anastomosis (arrowhead), and outflow cephalic vein (curved arrow). C, Endogenous transposed brachiobasilic fistula.
Note the inflow brachial artery, arteriovenous anastomosis, and the transposed basilic vein.
MAJOR DISORDERS
B
FIGURE 19-4 Endogenous radiocephalic arteriovenous fistula.
A, Multiple outflow stenoses. B, Improvement after using a 6-mm
angioplasty balloon.
Surveillance for AVFs depends on many of the same The 3-French (Fr) inner dilator of the micropuncture set
methods as those used for grafts. Physical examination allows diagnostic angiography and minimizes the risk
is very helpful and may be even more informative than for complications.37-41 Direct arterial access also allows
with grafts.32 Ultrasound can be used both preopera- evaluation of the palmar arch and antegrade or retrograde
tively to increase the rate of successful fistula place- filling of the distal segment of the artery feeding the fis-
ments33 and to evaluate fistula maturation.34 The other tula.37 After the diagnostic study has been performed, the
measures of graft function (recirculation, increased static fistula can be cannulated by a retrograde approach.37
venous pressures, decreased flow rates) are also evi- Venous stenoses in fistulas are seen with both immature
dence of fistula malfunction, but the thresholds for ab- and mature accesses. Turmel-Rodrigues and colleagues42
normality are not well established. As a result of the low think these venous stenoses must be dilated to at least
resistance and presence of the collateral veins, a venous 5 mm to obtain adequate flows.42 However, in a poorly
stenosis causes a reduction in blood flow in a fistula developed fistula, it may be important to perform serial
without the corresponding increase in access pressure.35 dilations, starting with undersized balloons (3 to 4 mm)
to avoid rupturing a small, fragile vein. If the vein is not
well developed, dilation with a small balloon during one
Endovascular Therapy
procedure and a repeat evaluation in 1 to 3 weeks with
PATIENT SELECTION dilation using a larger balloon may allow for develop-
The results of both percutaneous and surgical repair of ment of the venous outflow and maturation of the fistula
failing dialysis access are disappointing. Several studies (see discussion below). One of the more common sites of
have reported comparable primary patency rates at stenosis in a brachiocephalic fistula involves the cephalic
6 months (less than 25%) and 12 months.29,30 The NKF- arch region with a 39% prevalence of stenosis.43,44 This
KDOQI advises that each dialysis center determine region is less problematic with a radiocephalic fistula
which procedure is best for an individual patient based with an overall prevalence of 2%.43 Traditional angio-
on local expertise. Surgical revision is held to a higher plasty results within this region have been disappoint-
standard than percutaneous transluminal angioplasty, ing, with primary patency at 3, 6, and 12 months at 96%,
because surgical revision usually extends the access fur- 83%, and 75%, respectively.44 These outcomes have been
ther up the extremity by the use of a jump graft.1 in part due to the resistant nature of the stenosis, early
Although angioplasty is plagued with the same restenosis, high vein rupture rates, and other anatomic
problems with recurrent stenosis as surgery, it does and hemodynamic considerations.45
have some advantages. Patients accept percutaneous As many as 30% of native fistulas never mature to
balloon angioplasty better than they do a surgical pro- enable cannulation and allow for successful hemodi-
cedure. The angioplasty procedure avoids using a site alysis.46-49 If a fistula fails to mature over the first 1 to
further up the venous outflow, leaving it available for 3 months, early fistulography can enable identification
subsequent revision when it becomes necessary. The of an underlying stenosis for endovascular treatment
graft is immediately available for dialysis, avoiding the (Fig. 19-5). The initial salvage rate of nonmaturing
need for temporary dialysis catheters. Redilations al- AVFs ranges in the literature from 74% to 97%.50-57 Nu-
low easy and safe graft salvage for months or years.25 merous techniques have been used to improve fistula
New data also demonstrate promising results with function, including venous and arterial angioplasty,
stent grafts at graft-related stenoses.36 Percutaneous stent placement, thrombectomy, venous branch liga-
revision of venous anastomotic stenoses within a pros- tion, and fistula superficialization.58-59 In an effort to
thetic hemodialysis graft with the use of a stent graft increase the number of primary fistulas and expedite
appears to provide superior long-term patency than the use of a functional AVF, two new techniques have
standard balloon angioplasty. emerged, which include primary balloon angioplasty
during fistula creation (in selected patients with small
TECHNIQUE veins) and balloon-assisted maturation of immature
Dialysis graft/fistula venography should include a com- AVFs by angioplasty.60,61 These techniques allow use of
plete evaluation of the circuit from the inflow artery to the small or suboptimal veins to create functioning fistulas
superior vena cava. Access is usually done by palpation in within 2 months and increase overall functional AVF
the direction of suspected disease. Evaluation of fistulas rates to 90%.60,61
can be more complicated. A variety of techniques can be Venous anastomotic stenoses are the most common rea-
used to help with a difficult access. Real-time ultrasound son for malfunction of dialysis grafts. They usually oc-
guidance is extremely helpful. A tourniquet can be used to cur in the vein within a few centimeters of the
impede outflow and increase the size of the target veins. If graft-vein anastomosis (Figs. 19-6 and 19-7). At times,
direct fistula access fails, the brachial artery is punctured multiple venous channels may overlap and conceal im-
with a micropuncture needle central to the anastomosis. portant stenosis. Several oblique views may be required
19. HEMODIALYSIS ACCESS 585
A B
to visualize the narrowing. NKF-KDOQI guidelines rec- native fistulas.62 Some data may suggest longer inflation
ommend treating stenoses greater than 50% only when times are associated with less residual stenosis.62
there are concomitant clinical abnormalities and flow- If the stenosis does not yield to balloon dilation (resis-
rate reduction or pressure changes. After the stenosis is tant stenosis), repeated inflations may be required to open
found, it is dilated with an appropriately sized angio- the vessel. Multiple, prolonged inflations (e.g., 5 minutes)
plasty balloon catheter. Balloon diameter is generally are thought to be useful in resistant lesions. Cutting bal-
1 mm larger than the graft or 10% to 20% oversized com- loons have been used for extremely resistant stenoses63-67
pared to the adjacent normal vein. In the forearm and (Fig. 19-8). The devices have multiple microblades embed-
near the elbow, a 6- or 7-mm balloon typically is used ded in the balloon that incise the fibrotic vein wall and
initially. On occasion, veins may require 5- to 8-mm bal- allow successful angioplasty to follow. There is no evi-
loons. High-pressure balloons (burst pressures 20 to 30 dence that cutting balloons are superior to standard bal-
mm Hg) often are required to dilate these lesions. Very loons for simple stenoses.68 However, improved 6-month
high pressures (!20 atm) are more frequently needed in primary patency rates are noted for truly resistant lesions.69
586 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B
FIGURE 19-6 Venous anastomotic and intragraft stenoses.
A, Initial fistulogram through a catheter placed in the arterial limb
of the graft shows both lesions responsible for elevated venous
pressures at dialysis. B, After angioplasty with a 7-mm balloon, the
stenoses are relieved.
A A
D
FIGURE 19-9 Elastic stenosis within upper extremity fistula
treated with covered stent for salvage. A, Tight stenosis at basilic
vein transposition swing point. B, Stenosis treated with angioplasty
D but elastic recoil is evident. C, Patient presents 6 weeks later with
clotted fistula due to stenosis. After thrombus is removed, recurrent
elastic stenosis remains. D, Successful treatment with a Viabahn
covered stent. (Courtesy of W.L. Gore and Associates, Flagstaff, Ariz.)
Several projections may be required to adequately delin- Central venous stenoses are an important, although
eate the arterial inflow. If a significant arterial stenosis is less frequent, problem with hemodialysis grafts. Steno-
identified, angioplasty usually is indicated. The lesion sis of the subclavian and brachiocephalic veins usually
often can be reached through the access. Otherwise, a is caused by venous injury from prior dialysis catheters
direct brachial (or common femoral) arterial puncture is (Fig. 19-10). The importance of these obstructions is
necessary. In some cases, the arterial lesion is in the in- their potential to compromise future dialysis access
flow vessels, so arteriography should be considered dur- sites and to cause significant arm swelling. Outflow
ing the evaluation of a dysfunctional access, particularly stenoses should be treated with angioplasty only if they
if the patient has recurring graft dysfunction without an are considered to be responsible for graft dysfunction
evident cause.77,81 Measuring flow and pressures during (see Fig. 19-10). If the lesion is not causing symptoms,
percutaneous procedures may lead to increased detec- it should be left alone. Angioplasty of symptomatic
tion of arterial stenoses.77 central venous stenoses greater than 50% have been as-
Intragraft stenoses are relatively uncommon. These ste- sociated with more rapid stenosis progression of the
noses usually respond well to angioplasty (see Fig. 19-6). lesion.82 If a patient has a thrombosed graft, the most
Balloon sizing in the graft should take into account that likely culprit is a stenosis at the venous anastomosis.
these grafts are most commonly 6 mm in diameter. Oc- Unless the outflow is thrombosed up to the level of the
casionally the grafts also are tapered at the arterial anas- central vein, a central venous obstruction alone is prob-
tomosis (4 to 6 mm or 4 to 7 mm). In most cases a balloon ably not responsible for thrombosis. Near the shoulder
that is 1 mm larger than the graft diameter is an appro- and in the central veins, 10- to 12-mm balloons (or
priate size. If there is graft degeneration, it is particularly larger) may be necessary. The results of stent place-
important that a larger balloon not be used because the ment are not markedly better than those of balloon an-
graft can rupture. gioplasty in the central veins.83 The NKF-KDOQI and
A B
C
19. HEMODIALYSIS ACCESS 589
Society of Interventional Radiology guidelines recom- 23% and 20% in the balloon angioplasty group, respec-
mend transluminal angioplasty as the preferred treat- tively.36 In addition, freedom from subsequent inter-
ment for central vein stenosis, and stent placement is ventions at 6 months was significantly greater in the
indicated only with elastic lesions, when stenosis recurs stent graft group than in the balloon angioplasty group
within 3 months, or with occluded vessels1,84 (Fig. 19-11). (32% vs. 16%). Longer-term data are unavailable, but
The stent needs to be carefully oversized to avoid migra- stent grafts may have an important impact on future
tion.85-88 Balloon-expandable stents must be avoided at management of access grafts.
sites subject to extrinsic compression (e.g., subclavian Clinical results for dialysis AVFs are variable. The
vein running through the costoclavicular space). Stents initial salvage of nonmaturing AVFs ranges from 74%
should not be placed across the internal jugular or con- to 97% in the literature.50-57 One study of dysfunctional
tralateral innominate veins, which may be needed for fistulas had a primary, assisted primary, and secondary
future dialysis catheters. patency rates in 53 dysfunctional fistulas after inter-
vention at 3 months of 84% " 5%, 88% " 5%, and 90% "
RESULTS 4%, respectively. At 6 months, the patency rates were
Published series of nonthrombosed PTFE arteriovenous 55% " 8%, 80% " 6%, and 82% " 6%. At 12 months the
grafts have a reported 6-month primary (unassisted) rates were 26% " 11%, 80% " 6%, and 82% " 6%.95
patency of 40% to 50% after angioplasty.89-94 Repeated Turmel-Rodrigues reported a primary patency rate of
angioplasty enabled a primary assisted patency of 68% 39% and a secondary patency rate of 79% at 12 months
at 1 year and 51% at 2 years in one study. The secondary in dysfunctional forearm fistulas, and a rate of 57% in
patency rate (allowing for intercurrent thrombolysis patients with upper arm fistulas.96 Others have re-
and angioplasty) was 82% at 1 year and 65% at 2 years ported a 1-year secondary patency rate of 64% and a
in the same study. Although these patency rates seem 2-year secondary patency rate of 53%, with fewer pro-
low, they are comparable to results of operative treat- cedures to keep the fistulas functioning in comparison
ment. Based on such reports, NKF-KDOQI endorses with grafts.4
secondary patency rates after endovascular treatment In one report of 20 dialysis patients treated with
for dysfunction of at least 70% at 1 year, 60% at 2 years, stents in the central veins, primary patency rates of 90%
and 50% at 3 years.1 Primary unassisted patency (time at 1 month, 67% at 3 months, 42% at 6 months, and 25%
from one intervention to any other intervention to at l year were noted. Assisted primary patency (addi-
maintain patency) following angioplasty of failing tional angioplasty, stenting, or both) were 88% at
grafts should approach 50% at 6 months.1 The role of 3 months, 62% at 6 months, and 47% at 1 year in that
stent grafts for treatment of venous anastomotic graft series.97 Another study of 22 patients with a mix of stent
stenoses has shown promise, with recent data demon- devices showed primary patency rates after 3, 6, 9, and
strating 6-month treatment site and total access circuit 12 months of 82%, 73%, 56%, and 43%, respectively. The
patency of 51% and 38% in the stent graft group and primary assisted patency rates at the same time periods
A B
FIGURE 19-11 Treatment of recurrent central venous occlusion with stenting. A, Occlusion of the left brachiocephalic vein with neck
collaterals in a patient with a left upper extremity fistula. B, Successful stenting with 14-mm Wallstent with improved patency. (Courtesy of
Boston Scientific, Natick, Mass.)
590 V. MISCELLANEOUS VASCULAR INTERVENTIONS
COMPLICATIONS
Complications from endovascular treatment of dys-
functional dialysis access are uncommon. Most compli-
cations entail minor, self-limited bleeding or hematoma B
formation. Occasionally, damage to the veins may
occur, including rupture. Ruptures appear to be some-
what more common in autologous fistulas. The sig-
nificance of the vein rupture depends on the extent
of the leak. Because the angioplasty balloon should
already be in place, the balloon can be placed across
the rupture to seal the leak (Fig. 19-12). If prolonged
balloon inflation (5 to 10 minutes) does not seal the
rupture after two or three attempts, a bare or covered
stent should be considered50 (Fig. 19-13). If stenting is
not an option or ineffective, the operator may be C
forced to control the rupture by manual compression
of the access to achieve thrombosis. Vascular rupture
should occur only in 2% to 4% of cases, and perfora-
tion requiring blood transfusion, emergent surgery, or
limb-threatening ischemia should occur in fewer than
0.5% of cases.84
Surgical Therapy
Several surgical options are available for treatment of
obstructions that fail to respond to percutaneous inter-
ventions, including revision with patch grafting, a jump D
graft with extension of the graft farther up along the
FIGURE 19-12 Immature left upper extremity fistula with angio-
venous outflows, or complete graft replacement.105,106 plasty induced rupture treated with balloon tamponade. A, Tight
Revision is preferred over a new graft when feasible. stenosis within the left axillary vein. B, Stenosis relieved with
Replacement has the disadvantage of exhausting access angioplasty using an 8-mm balloon. C, Active extravasation after
sites much more rapidly. The 1-year primary patency angioplasty. D, After two rounds of prolonged (e.g., 5 to 10 minutes)
rate after surgical revision is as low as 25%, with a balloon inflation, no evidence of residual stenosis or extravasation
is seen.
secondary patency rate reported at 60% to 70%.106,107
Most grafts require multiple additional procedures to
maintain patency.
19. HEMODIALYSIS ACCESS 591
A B
Endovascular Therapy
Thrombosed Dialysis Fistulas and Grafts PATIENT SELECTION
Etiology Virtually all patients with clotted dialysis access are
In most cases, graft thrombosis occurs because of pro- candidates for percutaneous therapy. Unique charac-
gressive stenosis in the graft circuit (usually at the teristics of dialysis grafts make them particularly suit-
venous end). The goal of graft or fistula surveillance able for this approach. They are easy to access because
is to identify and repair lesions that threaten access of their superficial location, they contain fresh clot
patency. It is much easier and less expensive to cor- (usually not more than 48 to 72 hours old), and they are
rect a venous stenosis than to have to declot the graft/ a closed system with only a single inflow and (some-
fistula and then correct the venous stenosis that caused times) outflow. The criteria for rejecting patients for
the thrombosis. Occasionally, dialysis access will clot pharmacologic graft thrombolysis are similar to those
because of hypotension, graft infection, trauma, or a for other thrombolysis procedures. If pharmacologic
hypercoagulable state. therapy is not appropriate, mechanical thrombolysis
592 V. MISCELLANEOUS VASCULAR INTERVENTIONS
can be used. Absolute contraindications to pharmaco- needle or micropuncture needle (Cook, Inc., Blooming-
logic therapy include recent cerebrovascular process/ ton, Ind.) is used to access the graft. The first puncture is
disease/procedure (tumor, recent stoke, trauma, sur- made toward the venous anastomosis. Puncturing the
gery) or active gastrointestinal bleeding. Relative con- graft sometimes is difficult because of scar tissue from
traindications include major surgery or organ biopsy repeated dialysis needle puncture. It is helpful to hold the
within 2 weeks, recent serious trauma, preexisting un- graft firmly between the thumb and fingers of one hand
correctable coagulation defects, uncontrolled severe while puncturing the graft with the needle held in the
hypertension, and pregnancy. other hand. When the needle passes through the graft
Dialysis graft infection is an important contraindica- material, usually there is a popping sensation or loss of
tion to any type of thrombolysis. Lysis of infected clot resistance, although if scar has developed, this sensation
can precipitate bacteremia and lethal sepsis. Determin- may be diminished. There usually is little or no blood re-
ing whether a graft is infected can be difficult.108 Classic turn when a thrombosed graft is entered. When the nee-
signs of infection (i.e., redness, tenderness, warmth, dle is in the graft, a guidewire normally passes easily. If
swelling, and fever) may be subtle or absent in patients the patient complains of pain with the guidewire passage
with chronic renal failure. Definite signs of infection, or the wire fails to follow the course of the access, the guide-
such as a purulent discharge or skin breakdown over the wire probably is extraluminal. The needle is removed and
graft, are rare. Needle aspirates of graft clot or fluid col- a sheath placed. A guidewire is then advanced beyond
lections around the graft can be sent for Gram stain and the venous anastomosis and into the venous outflow.
culture.109 Infection of the graft requires treatment with If the guidewire and catheter cannot be manipulated
antibiotics and referral for surgical removal. into the venous outflow, the procedure should be termi-
Small pulmonary emboli are produced during most nated. Attempting thrombolysis in the face of an impass-
percutaneous dialysis graft declotting procedures.110-112 able venous obstruction leads to bleeding when inflow
Although most patients tolerate these emboli, patients is reestablished. In this situation, the patient is referred
with significant pulmonary hypertension or severe un- for thrombectomy and surgical revision of the venous
derlying lung disease may not. A known right-to-left anastomosis.
cardiac shunt (which could result in embolic stroke) is a A small amount of contrast is injected through the
strict contraindication to any type of lysis procedure. catheter, and the catheter is withdrawn until the venous
Grafts that fail within days to several weeks of place- end of the thrombus is identified. The length of the
ment usually have a technical problem responsible for thrombosed segment, from the venous end of the clot to
thrombosis. Although the graft may not be salvageable the entrance site into the graft, is determined. A pulse-
with percutaneous therapy, thrombolysis or simple con- spray catheter with appropriate length of side holes is
trast injection of the venous anastomosis and outflow placed into the graft.
veins may help guide surgical revision. Although some The arterial end of the graft is approached in a similar
risk of hemorrhage from the anastomoses exists, manual manner. The needle is placed into the graft a short dis-
compression usually controls such bleeding. tance away from the venous end of the graft and di-
rected toward the arterial end. A pulse-spray catheter is
PULSE-SPRAY THROMBOLYSIS positioned with the end hole just beyond the arterial
There are several methods for administering thrombolytic anastomosis. It is important to manipulate guidewires
agents into dialysis grafts. One of the techniques described and catheters gently at the arterial end of the graft.
relatively early in experience of treating dialysis grafts Forceful, vigorous motion of the wire or injection of con-
with thrombolysis was pulse-spray pharmacomechanical trast may dislodge clot into the feeding artery.
thrombolysis (PSPMT). Although perhaps supplanted by The most commonly used thrombolytic in the United
more recently described thrombolytic approaches, PSPMT States for dialysis grafts is recombinant tissue-type plas-
remains a good technique, particularly for those who are minogen activator (t-PA) 2 mg dissolved in 5 to 10 mL
just gaining experience in graft thrombolysis. If another of normal saline.115-117 Reteplase (a genetically altered ver-
thrombolytic approach is ineffective, this method can be sion of t-PA) is also effective, typically in a dose of 1 to
used to salvage the situation. 3 units in 5 to 10 mL of saline.118 Patients also receive
Several catheter systems are suitable for PSPMT (e.g., 3000 to 5000 units of IV heparin. The thrombolytic solu-
Unifuse catheter). These devices have multiple side holes tion is divided equally between two syringes. Aliquots
or slits over lengths of 5 to 40 cm. A tip-occluding wire is of 0.2 to 0.3 mL of solution are injected into each catheter
used to obstruct the catheter endhole. All of the devices over about 10 minutes. Forceful injection enhances the
allow a high-pressure fluid spray to be delivered into the diffusion of the thrombolytic agent into the clot and pro-
substance of the clot. To lyse the entire clot and treat the duces some mechanical disruption of the clot matrix,
arterial and venous ends of the grafts, a crossed catheter increasing the surface area exposed to the thrombolytic
technique is used78,113,114 (Fig. 19-14). A single-wall, 18-gauge agent.119 One dose of thrombolytic solution is sufficient
19. HEMODIALYSIS ACCESS 593
A B
to treat most hemodialysis grafts. The graft may have platelets and fibrin.120,121 Because these plugs are rela-
only a weak pulse despite near-complete lysis because tively resistant to thrombolysis, further thrombolytic
of resistant clot at the arterial end. Small to moderate treatment is of little value. Mechanical dislodgment and
volumes of residual clot at other sites do not require maceration of the plug is much more effective. Throm-
further thrombolytic therapy. Large amounts of residual bectomy is performed using compliant balloons that can
clot may indicate incomplete treatment of the entire clot, exert force and traction on the plug as it is pulled out of
insufficient heparinization, or infected thrombus resis- the arterial anastomosis (Fig. 19-16). These balloons in-
tant to thrombolytic agents. clude an 8.5-mm occlusion balloon catheter (Boston Sci-
Contrast injection through the venous catheter with- entific, Watertown, Mass.) or an over-the-wire Fogarty
drawn below the anastomosis demonstrates a stenosis in balloon catheter (Baxter, Irvine, Calif.). Maceration with
most cases. The venous stenosis is treated with balloon a dilation balloon at the arterial anastomosis is avoided
angioplasty to provide graft outflow before graft inflow because of the risk of arterial embolization or injury. It is
is addressed. In many cases, a lysis-resistant clot remains important to avoid overinflation of the balloon in the na-
at the arterial anastomosis (Fig. 19-15). This arterial tive artery. If the balloon is overexpanded, the balloon
plug is probably composed of densely packed layers of may rupture or damage to the artery may result. Two or
594 V. MISCELLANEOUS VASCULAR INTERVENTIONS
MECHANICAL THROMBECTOMY
Multiple mechanical thrombectomy devices are ap-
proved by the U.S. Food and Drug Administration for
treating dialysis grafts, including the AngioJet infusion
system, Arrow-Trerotola Percutaneous Thrombec-
tomy Device (PTD), Akonya Eliminator, Castaneda
Over the Wire Brush, Helix Clot Buster Thrombectomy
(Amplatz Device), Oasis Thrombectomy System, Prolu-
men, Thrombex PMT, and X-Sizer Catheter System.
Thrombectomy devices have a variety of methods for
removal of clot. Some cause clot fragmentation by pro-
ducing a vortex created by a high-speed rotating impel-
ler or basket.124 Others work by Venturi effect, in which
FIGURE 19-15 Lysis-resistant plug on the graft side of the thrombus is sucked into the aperture of the device and
arterial anastomosis (arrow). Contrast has been injected into the macerated by high local shear forces. The fragments are
proximal graft and feeding radial artery after inflating the occlusion removed through an exhaust lumen.124 Heparin (3000
balloon.
to 5000 units in most cases) is commonly infused
through the sheath before the thrombectomy device is
placed.125 If it is not given through the sheath, it should
three passes may be necessary to completely remove the be given intravenously.
clot. When the plug is displaced from the anastomosis, it The approach to using these devices is similar to
may become trapped in the graft, usually at the site that for pulse-spray thrombolysis. Vascular sheaths of
where the catheters enters the graft. In this situation, an appropriate size are required. Some operators do not
angioplasty balloon is used to fragment the clot. Any open the venous stenosis until after performing the
other residual clot in the graft also is macerated with an thrombectomy, whereas others perform angioplasty at
angioplasty balloon. the venous end to allow outflow and to decrease the
After flow has been established, the entire graft circuit risk of increased pressure, which itself could lead to
from the arterial inflow to the superior vena cava is stud- arterial emboli.125 Contrast can be injected through the
ied with venography for other obstructions. If the patient sheath to visualize the clot. After the clot is removed
is going to dialysis immediately, short 7-Fr dialysis from the venous end, the venous stenosis is dilated.
sheaths are placed. Otherwise, an activated clotting time After the venous angioplasty, the venous end of the
is obtained to assess the patients anticoagulation status graft is punctured in the direction of the arterial end.
before removing the catheters. The thrombectomy device is then advanced to clear
the clot at the arterial end. An occlusion balloon is
LYSE AND WAIT METHOD placed to dislodge the arterial plug. Following this
The lysis and wait technique was first described by maneuver, the graft is assessed with contrast to deter-
Cynamon and colleagues.122,123 An Angiocath or micro- mine whether the procedure is complete or whether
puncture set is inserted into the arterial end of the graft other areas require therapy (Fig. 19-17).
by means of ultrasound or palpation. The graft is manu- Some operators prefer to use a single puncture at the
ally compressed at the arterial and venous anastomoses apex of a loop graft as the access point and then direct
while the thrombolytic mixture (t-PA 2 mg in 5 to 10 mL the sheath toward the limb of the graft that requires
normal saline) is slowly infused over 1 minute.115,116,123 treatment. Other operators pull the arterial plug back
This portion of the procedure can be accomplished in a into the graft early in the procedure, before treating the
19. HEMODIALYSIS ACCESS 595
A B
RESULTS
venous stenosis, so the plug can be fragmented by the All three methods of treatment are similarly effective for
mechanical device.125 clotted dialysis grafts, with initial clinical success (i.e.,
ability to undergo at least one session of dialysis) of
ARTERIOVENOUS FISTULA THROMBOSIS greater than 90% with a NKF-KDOQI clinical success rate
AVF thrombolysis is much more challenging than graft goal of 85%.* The overall procedure time is usually less
thrombolysis.126-128 Ultrasound is used to confirm that than 2 hours. The different mechanical thrombectomy
the fistula is truly thrombosed rather than harboring a devices seem to be relatively comparable in their reported
stenosis that results in poor flow and subsequent flat- success rates; they all remove clot, and differences may be
tening of the fistula (see earlier discussion). Depending largely a function of operator experience.125,134,135 The
on the anatomy, fistulas may be accessed using ante- technical success results are comparable between devices,
grade and/or retrograde approach. As with dialysis and pharmacologic thrombolysis and patency rates at
grafts, pulse-spray, lyse and wait, and mechanical 1, 3, and 6 months also are comparable.116,134-140
devices have been used.126,129-132 Direct thromboaspira- Long-term primary patency of thrombosed dialysis
tion of the fistula may be successful.91 This method can grafts is relatively poor whether grafts are treated by
be performed with 7- or 8-Fr, thin-walled aspiration PSPMT, mechanical devices, or surgical thrombectomy and
catheters and a 20-mL syringe to provide the aspiration
suction.124,133 *See references 1, 78, 84, 96, 108, 109, 113, 115-118, 132-140.
596 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B
revision. For enzymatic thrombolysis, the primary patency arterial embolization, and vein rupture from angio-
rate at 1 year is 11% to 26% and secondary patency rate at plasty.147 The complication rates for most of the me-
1 year is 51% to 69%.114 Studies directly comparing surgical chanical devices are similar. Bleeding from previous
thrombectomy with thrombolysis and angioplasty demon- needle punctures is seen occasionally, particularly when
strate similar patency rates. However, reocclusion rates are the venous outflow stenosis is not treated before flow
similar following multiple declotting procedures, regard- is reestablished. In this situation, pressure is applied
less of the technique used, so continual percutaneous man- to the bleeding site, and the venous outflow is opened
agements should be undertaken to preserve each graft for expeditiously.
as long as possible.132 Even if grafts rethrombose early Embolization into the arterial system occurs in up to
(within 2 months), aggressive retreatment of these grafts, 10% of procedures.84 Further thrombolysis of these
commonly using a larger angioplasty balloon, or occasion- emboli (which usually arise from the arterial plug) is
ally stent placement allowed salvage of the grafts without often ineffective, and mechanical removal is required
significantly decreased patency rates.141 when clots are symptomatic or arterial supply to the
Endovascular treatment of thrombosed dialysis fistu- hand is compromised. After determining the location
las is quite effective, with technical success rates for de- of the embolus, a wire is placed past the arterial anas-
clotting fistulas ranging from 75% to 100%. Primary pa- tomosis and past the embolus. An occlusion balloon
tency rates are reported to be 36% to 70% and 18% to catheter is placed from the graft into the artery beyond
60% at 3 and 6 months, respectively, with 60% to 80% the clot, and the clot is pulled back into the graft. If the
assisted primary patency rates at 6 months.126,142-146 De- graft is patent, the back-bleeding technique can be
clotting of fistulas may involve multiple modalities such tried.148 The graft must first be patent. A balloon cath-
as thrombolytics, thromboaspiration, mechanical throm- eter is placed into the arterial inflow, just above the
bectomy, and angioplasty. anastomosis, on the upstream side. The balloon is in-
flated, and the patient exercises the hand for about
COMPLICATIONS 1 minute. The balloon is deflated and an arteriogram is
Major and minor complications of thrombolysis for di- performed to evaluate the results. A successful proce-
alysis access occur in about 1% and 10% of cases, respec- dure dislodges the embolus from its position in the
tively.84 Most complications involve perigraft bleeding, artery below the anastomosis and into the graft.149
19. HEMODIALYSIS ACCESS 597
Small pulmonary emboli are produced with all percu- flow reversal may result in a clinically significant steal. A
taneous declotting techniques.109-111,139,150,151 Symptomatic second cause for distal ischemia is occlusive disease in the
pulmonary embolism is rare. However, fatal pulmonary inflow arteries.81 The combination of decreased inflow and
embolism has been reported after mechanical throm- shunting of blood through the graft leads to ischemic hand
bectomy in which the entire clot burden of a graft was symptoms.
delivered to the lungs.140,150 A patient with dialysis graft-related ischemia has a cool,
pale extremity. Trophic changes of the skin and nails or
muscle wasting may develop. The patient may complain
OTHER DISORDERS of numbness, tingling, impairment of motor function, or
pain on exertion of the hand. The symptoms often are
worse during dialysis.152 In more severe cases, numbness
Ischemia and Steal Syndrome and pain progress, with diminished sensation, muscle and
Dialysis fistulas/grafts create a low-resistance circuit be- nerve paralysis, ischemic ulcers, and progressive dry gan-
tween the arterial and venous systems. Most patients toler- grene of one or more affected digits.152
ate this physiology without difficulty, but some patients The diagnosis of ischemia can be made in several
may develop distal limb ischemia. The incidence of isch- ways, including digital plethysmography, pulse oximetry,
emic complications ranges between 1% and 10%.152-154 The and segmental pressure measurements.154 A significant
most common cause is high resistance in the arterial bed decrease in blood pressure along the extremity indicates
beyond the arteriovenous anastomosis, with shunting of an obstruction in the arterial circulation at this site. Pulse
blood into the graft. A steal from the ulnar artery through volume recordings documenting digital pressures less
the palmar arches causes reversed flow in the distal radial than 50 mm Hg and augmentation of the pulse wave with
artery, shunting of blood away from the peripheral tissues, fistula compression are diagnostic of vascular steal.152,154
and resulting hand ischemia (Fig. 19-18). This situation is Digital pulse oximetry also has proven useful in diagnos-
most common in patients with coexisting small vessel ing vascular accessassociated steal. Oxygen saturations
disease such as diabetes, vasculitis, or peripheral vascular are low, but they rise to normal levels when the fistula is
disease.154 In these patients, even mild degrees of arterial compressed.152 Angiography can be performed to identify
A B
FIGURE 19-18 A, Injection in the brachial artery demonstrates filling of the ulnar artery (black arrow), and filling of the radial artery
(arrowhead) that directly supplies the dialysis access (white arrow). B, Later in the injection, the distal radial artery (arrowhead) shows marked
filling in a retrograde fashion from the palmar arch.
598 V. MISCELLANEOUS VASCULAR INTERVENTIONS
Venous Hypertension
Obstruction of dialysis access venous outflow may lead
to retrograde, high-pressure flow through collateral veins
and result in venous hypertension. This situation is most
common with upper arm fistulas when there is occlusion
of central veins. Patients suffering from venous hyper-
tension have edema, cyanotic discoloration, and, with
long-standing hypertension, pigmentation changes of
the skin.156 Dilated, tortuous collateral veins are observed
in the extremity and often across the chest. Swelling of
the extremity causes pain and impaired function and B
may lead to ischemic ulceration.156
FIGURE 19-19 A, Angiogram shows a large graft pseudoaneurysm.
Patients should be evaluated before graft placement if B, The lesion was repaired by off label placement of a covered Flair
they have preexisting arm edema, collateral vein devel- stent. (Courtesy of Dr. Carr, Boise, Idaho.)
opment, history of subclavian vein catheters or pace-
maker placement, or trauma to the extremity.157 Imaging
is done with duplex ultrasound or magnetic resonance
imaging.158,159 If symptoms of venous hypertension occur spontaneous bleeding, or infection. Surgery usually in-
after access creation, a venogram should be performed. If volves resection of the pseudoaneurysm and interposi-
there is a central venous stenosis or occlusion, angio- tion or bypass grafting around the lesion. More recently,
plasty and possibly stenting (for an occlusion) should be stent grafts have been used to treat patients with pseu-
attempted. In many cases, angioplasty resolves the arm doaneurysms of aging, degenerating dialysis grafts and
swelling at least for 3 to 6 months, then repeated angio- aneurysms of AVFs73,160-162 (Fig. 19-19). In one of the larg-
plasty can be performed, which can prolong the use of est series, Vesely162 used Viabahn stent graft placement
the access sometimes for years.25 for graft-related pseudoaneurysms with reported pri-
mary patency of 71% at 3 months and 20% at 6 months.
Aneurysms and Pseudoaneurysms
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61. De Marco Garcia LP, Davila-Santini LR, Feng Q, et al. Primary bal- 84. Aruny JE, Lewis CA, Cardella JF, et al. Quality improvement
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Interv 2003;58:524. 90. Beathard GA. Percutaneous transvenous angioplasty in the treatment
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Radiol 2004;15:1463. nosis and thrombosis in haemodialysis fistulas and grafts by inter-
67. Singer-Jordan J, Papura S. Cutting balloon angioplasty for primary ventional radiology. Nephrol Dial Transplant 2000;15:2029.
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68. Vesely TM, Siegal JB. Use of the peripheral cutting balloon to treat Am J Kidney Dis 2001;37:945.
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69. Wu CC, Lin MC, Pu S, et al. Comparison of cutting balloon versus stenosis: A nephrologists view. Semin Dial 1995;8:166.
high pressure balloon angioplasty for resistant venous stenoses of 94. Katz SG, Kohl RD. The percutaneous treatment of angioaccess
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70. Trerotola SO, Ponce P, Stavropoulos SW, et al. Physical examina- 95. Clark TW, Hirsch DA, Jindal KJ, et al. Outcome and prognostic factors
tion versus normalized pressure ratio for predicting outcomes of of restenosis after percutaneous treatment of native hemodialysis fistu-
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71. Sapoval MR, Turmel-Rodrigues LA, Raynaud AC, et al. Cragg 96. Turmel-Rodrigues L, Pengloan J, Baudin S, et al. Treatment of ste-
covered stents in hemodialysis access- initial and mid-term results. nosis and thrombosis in haemodialysis fistulas and grafts by inter-
J Vasc Interv Radiol 1996;7:335. ventional radiology. J Vasc Interv Radiol 2002;13:51.
72. Bent CL, Rajan DK, Tan K, et al. Effectiveness of stent-graft place- 97. Vesely TM, Hovsepian DM, Pilgram TK, et al. Upper extremity
ment for salvage of dysfunctional arteriovenous hemodialysis central venous obstruction in hemodialysis patients: treatment
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73. Silas AM, Bettmann MA. Utility of covered stents for revision of 98. Maskova J, Komarkova J, Kivanek J, et al. Endovascular treatment
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74. Lin PH, Johnson CK, Pullium JK, et al. Transluminal stent graft 99. Funaki B, Szymski GX, Leef JA, et al. Wallstent deployment to sal-
repair with Wallgraft endoprosthesis in a porcine arteriovenous vage dialysis graft thrombolysis complicated by venous rupture:
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100. Clark TW. Nitinol stents in hemodialysis access. J Vasc Interv Radiol 121. Winkler TA, Trerotola SO, Davidson DD, Milgrom ML. Study of
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101. Vogel PM, Parise C. SMART stent for salvage of hemodialysis 1995;197:461.
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102. Gray RJ, Horton KM, Dolmatch BL, et al. Use of Wallstents for ting: description of the lyse and wait technique. J Vasc Interv
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untreatable with balloon angioplasty. Radiology 1995;195:479. 123. Cynamon J, Pierpont CE. Thrombolysis for the treatment of
103. Vogel PM, Parise C. Comparison of SMART stent placement for thrombosed hemodialysis access grafts. Rev Cardiovasc Med 2002;
arteriovenous graft salvage versus successful graft PTA. J Vasc 3(Suppl. 2):S84.
Interv Radiol 2005;16:1619. 124. Morgan R, Belli AM. Percutaneous thrombectomy: a review. Eur
104. Hoffer EK, Shahnaz S, Herskowitz MM, et al. Prospective random- Radiol 2002;12:205.
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105. Bitar G, Yang S, Badosa F. Balloon versus patch angioplasty as an Radiol 1999;2:208.
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108. Davis GB, Dowd CF, Bookstein JJ, et al. Thrombosed dialysis grafts: urokinase infusion for the restoration of function in thrombosed
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109. Valji K, Roberts A, Bookstein J. Thrombosed hemodialysis access tion of occluded haemodialysis fistulae with the Hydrolyser
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C H A P T E R
20
Neurointerventions
Tony P. Smith
ANATOMIC AND TECHNICAL are individualized for a particular patient and his or
CONSIDERATIONS her unique clinical situation. Coils and particles of vari-
ous sizes are the most often used. Pushable standard
Multiple sources describe the angiographic anatomy of coils (0.035 and 0.038 inch) are used to occlude large
the cerebrovascular system1,2 (Fig. 20-1). Interestingly, vessels such as the vertebral or carotid arteries, as well
large portions of the anterior (carotid) and posterior as larger branches of the external carotid artery (ECA).
(vertebrobasilar) circulations supply areas of the brain However, most neurointerventionalists are more com-
in which little is understood regarding functionality. fortable with the precision and safety of electrolytically
In effect, one may occlude a large vessel as seen by or mechanically detached coils.4 Now that detachable
angiography, resulting in essentially no clinical neuro- balloons are no longer available in the United States,
logic change. Alternatively very small vessels may sup- occlusive plugs are gaining favor for rapid occlusion of
ply highly important areas where vessel occlusion may large vessels.5 Particulate agents (polyvinyl alcohol
manifest as major neurologic deficits. In addition, [PVA] and gelatin microspheres) are used for small
whenever an artery is occluded, the clinical neurologic artery occlusion, such as in epistaxis or preoperative
result not only depends upon the functionality and tumor embolization.6 If the operator can place the micro-
degree of cerebral tissue supplied, but also the presence catheter close to the tumor bed, particles of very small
and degree of collateral circulation. These collaterals size (e.g., 50 to 100 microns) are appropriate. However,
can at times be troublesome, particularly during exter- larger particles are also used if there is particular con-
nal carotid embolization, where they may supply the cern for nontarget embolization, especially of neural
intracranial circulation3 (Table 20-1). tissue or skin. Liquid agents such as cyanoacrylate,
Diagnostic angiography of the brachiocephalic vessels ethylene vinyl copolymer (Onyx Liquid Embolic System,
is performed using 4- or 5-French (Fr) catheters. These eV3 Neurovascular, Irvine, Calif.), and sclerosants are
catheters have 0.038-inch lumens, which accommodate more commonly used extracranially for facial arterio-
microcatheters, even of the larger lumen and higher flow venous malformations.7
variety. However, once the microcatheter is in place, Angioplasty and stenting of the extracranial and in-
contrast injections through the diagnostic catheter for tracranial vessels has gained popularity. Stent place-
angiographic runs or subtracted fluoroscopy are very ment at the carotid artery bifurcation is performed
limited. For that reason, most embolization procedures today through a variety of 6-Fr, 90-cm long sheaths,
use a guiding catheter, with 6 Fr being the most common. permitting insertion of stents up to 10 mm in diameter.
This device easily accommodates a microcatheter while Angioplasty of smaller arteries such as the intracranial
reserving ample guiding catheter lumen for contrast in- vessels is usually performed via 6-Fr guiding catheters
jections, permitting angiographic runs and high-quality using coronary artery balloons and either specialized
subtracted fluoroscopic imaging. The latter is an integral self-expanding intracranial stents or balloon-expandable
part of extracranial and intracranial catheterizations. Just coronary stents, all of which track over 0.014-inch
as for the peripheral circulation, guiding catheters come guidewires.
in a variety of shapes and microcatheters in a variety of Angioplasty and stenting of the extracranial internal
sizes. The microcatheter should be sized appropriately carotid artery is carried out using embolic protection
for the intended embolic agent. devices to prevent embolization to the intracranial cir-
As in the peripheral circulation, all embolic agents culation. Embolic protection involves either deploy-
are carefully chosen based on the disease process, and ment of a filter beyond (above) the lesion or inflation of
603
604 V. MISCELLANEOUS VASCULAR INTERVENTIONS
10
10
9
9
7
L 13 A
6 3 3 6
2 2 2
5 1 8 4 *
* 13
4
8
1
1 1
A B C
13 13
4
13
16 16 4 mma
13
12
16 1
15 21 22
15 mma 20
12 20
SP
15
14
20
14 23
14 14
11
17 18
19
11
D E F 18 G
FIGURE 20-1 Normal craniofacial arterial distribution. Arteries: 1, internal carotid artery; 2, middle cerebral artery (M1); 3, anterior
cerebral artery (A1); 4, posterior communicating artery; 5, anterior communicating artery; 6, M2 branches of the middle cerebral
circulation; 7, A2 branches of the anterior cerebral circulation; 8, ophthalmic artery; 9, pericallosal artery; 10, callosomarginal artery; 11,
vertebral artery; 12, basilar artery; 13, posterior cerebral (P1) artery; 14, posterior inferior cerebellar artery (PICA); 15, anterior inferior
cerebellar artery (AICA); 16, superior cerebellar artery; 17, external carotid artery; 18, facial artery; 19, lingual artery; 20, occipital artery;
21, superficial temporal artery (STA); 22, internal maxillary artery (IMax); 23, ascending pharyngeal artery; A, angular artery; M, motor
cortex; mma, middle meningeal artery; SP, sphenopalantine artery; *, anterior choroidal artery. A, Early phase of a right internal carotid
artery angiogram in an anterior-posterior projection. Note the filling of the anterior communicating artery (5), which allows flow from the
right to the left anterior (carotid) distributions. There is a very small amount of back-filling into the left distal intracranial carotid artery (1).
The left internal carotid artery in this patient was normal by angiography. The lenticulostriate arteries (L), although small, provide
important blood supply to the internal capsule. The patient has a patent posterior communicating artery giving supply to the posterior
cerebral circulation (13) on the right. B, Early phase of a right internal carotid artery angiogram in a lateral projection. Posterior communi-
cating artery (4) supplying the posterior cerebral artery is well seen. The ophthalmic artery (8) is best seen on the lateral projection. C, Later
phase of a right internal carotid artery angiogram in a lateral projection. This is a different patient than in B. The posterior cerebral artery
(13) has a complete origin from the carotid artery, although its first portion is often referred to as the posterior communicating artery (4).
The double asterisks (**) represent the anterior choroidal artery, which in its proximal portion supplies the anterior limb of the internal
capsule. The motor cortex in the posterior frontal lobe is estimated to be at the area marked by M. D, Left vertebral artery angiogram in the
frontal view. The patient does not have a right vertebral artery. Therefore the left posterior inferior cerebellar artery (PICA) (14) supplies the
right PICA (14) as well. E, Left vertebral artery angiogram in the lateral view. Note the bilateral posterior communicating arteries (4). F, Left
external carotid artery injection in the lateral view. A small amount of reflux of contrast material is seen in the internal carotid artery (1).
Note that most of the vessels of the external carotid artery distribution are better seen on the lateral projection. This is an early phase
injection and the normal, small middle meningeal artery (mma) is faintly visualized. G, Left external carotid artery injection in the frontal
view. Branches of the distal internal maxillary artery (22) and portions of the occipital artery are seen well in the frontal view. The delicate
sphenopalantine (SP) artery branches are seen. These are the branches targeted in patients undergoing embolization for epistaxis.
EXTRACRANIAL INTRACRANIAL
From Geibprasert S, Pongpech S, Armstrong D, et al. Dangerous extracranial-intracranial anastomoses and supply to the cranial nerves: vessels the neurointerventionalist needs
to know. AJNR Am J Neuroradiol 2009;30:1460.
AMA, accessory meningeal artery; CN, cranial nerve; ICA, internal carotid artery; ILT, inferolateral trunk; MMA, middle meningeal artery.
Table provides the major extracranial artery and the location along its course where an extracranial branch potentially anastomoses with an intracranial branch supplying an
important intracranial artery.
A B C D
FIGURE 20-2 Cervical carotid artery angioplasty and stenting in a 74-year-old man with occluded right internal carotid artery and
prior left cerebral transient ischemic attack. A, Anteroposterior view of left carotid bifurcation demonstrates a 60% narrowing of the
proximal internal carotid artery (arrow) with ulceration and narrowing of the proximal external carotid artery as well. B, Anterior posterior
angiogram of the left carotid bifurcation after angioplasty and stent placement. No residual stenosis is noted at the proximal internal
carotid artery (arrow). Note the distal protection device (arrowhead) in a relatively straight segment of the internal carotid artery. C, Filter-
Wire EZ distal protection device used in the patient shown in B. Note that the protection device is part of the guidewire and the mesh is
radiolucent but fixed to a radiopaque ring inferiorly (arrowhead). D, Angioguard Emboli Capture Guidewire. Note that there are a number
of designs for distal protection devices. (C, Courtesy of Boston Scientific, Natick, Mass., with permission. D, Courtesy of Cordis, Miami Lakes,
Fla., with permission.)
606 V. MISCELLANEOUS VASCULAR INTERVENTIONS
now approval from the U.S. Food and Drug Adminis- 600 mg) early on the day of the procedure. This combi-
tration for all patients with significant cervical carotid nation therapy is maintained for 1 month after stent-
artery stenoses regardless of symptomatology or suit- ing; one antiplatelet agent (usually aspirin) is contin-
ability for surgery (Box 20-1). For the great vessel origins ued without interruption indefinitely. For the procedure
and the extracranial vertebral artery, endovascular tech- itself, heparin (or a direct thrombin inhibitor in allergic
niques are often preferred over operation. patients) is administered to achieve an activated clot-
Before angioplasty and stenting of the cephalic ves- ting time of at least twice what is normal (e.g., 250 to
sels, antiplatelet and anticoagulation therapy is essen- 300 seconds.)
tial. Experimental and clinical data from animal mod- Contraindications specific to carotid and vertebral ar-
els and human coronary intervention suggest that tery stenting are relative and include inability to tolerate
aspirin and clopidogrel (Plavix) have a synergistic antiplatelet therapy and recent stroke. The latter exclu-
effect on inhibition of platelet aggregation, antithrom- sion criterion is based on experience with CEA, where
botic activity, and prevention of myointimal prolifera- revascularizing the inflow to areas of acutely infarcted
tion.20,21 Therefore patients receive a dual antiplatelet cerebral tissue may result in intracranial hemorrhage.22
regimen consisting of aspirin (81 or 325 mg daily) and
clopidogrel (75 mg daily). This treatment is started at TECHNIQUE AND RESULTS
least 5 days before the procedure or given as a loading Endovascular treatment of the origins of the great vessels
dose of aspirin (325 to 700 mg) and clopidogrel (300 to often focuses upon the left subclavian artery, the com-
mon location for lesions resulting in subclavian steal
syndrome (see later discussion). However, the same
principles hold for the origins and proximal regions of
BOX 20-1
the right brachiocephalic and left common carotid arter-
HIGH-RISK CRITERIA ies. Although the latter two treatment sites are often
FOR CAROTID grouped in publications with the left subclavian artery,
E N D A RT E R E C T O M Y their outflow into the internal carotid arteries entails
added risks from embolic events.
Constitutional Arterial access can be either transfemoral or via a
retrograde arm approach. It is thought that the arm ac-
Clinically significant cardiac disease cess enhances success in crossing total occlusions due to
Multivessel coronary artery disease, severe the proximity of the access site to the lesion as well as a
angina, LVEF 30% or less, heart failure, need more stable access via the distal subclavian artery rather
for open heart surgery than the aorta.
Severe pulmonary disease Atherosclerotic lesions involving the great vessels
FEV1 !50% often occur at or near their origins and are therefore
Age "80 years most often treated using stents.23,24 Angioplasty alone
may be undertaken in the midportions of these vessels
Anatomic but lesions located at the carotid bifurcation are cur-
Anatomically high bifurcation rently relegated to stenting. Balloon-expandable stents
Unable to position neck for surgery are often preferred to allow accurate device placement
Severe cervical spinal disease, cervical spine at the origin of the vessel (Fig. 20-3). Fortunately, bal-
fixation loon-expandable stents are generally not subject to ex-
Prior carotid endarterectomy trinsic compression and collapse at these locations
Contralateral carotid occlusion deep in the chest. Self-expandable systems are a rea-
Recurrent stenosis after endarterectomy sonable alternative, particularly if vessel tortuosity or
Contralateral laryngeal nerve palsy variations in vessel diameter are encountered. The use
Previous radical neck surgery of distal protection devices for proximal great vessel
Radiation therapy to the neck angioplasty is based on operator preference. The re-
sults of great vessel angioplasty for atherosclerotic
From Yadav JS, Wholey MH, Kuntz RE, et al. Protected lesions are excellent.25-27 Primary technical success
carotid-artery stenting versus endarterectomy in high-risk ranges from 93% to 99% with cerebral ischemic compli-
patients. N Engl J Med 2004;351:1493.
FEV1, forced expiratory volume in 1 second; LVEF, left
cations ranging from 2% to 3%. Long-term patency
ventricular ejection fraction. ranges from 93% at 1 year to 79% at 5 years.
All risks are relative and somewhat dependent on the particular The term subclavian steal is used when a significant
patient and surgeon.
stenosis or occlusion of the subclavian artery proximal to
the vertebral artery origin occurs (Fig. 20-4). Blood from
608 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B C
FIGURE 20-3 Great vessel angioplasty and stenting in a 75-year-old man with new onset blurred vision and transient ischemic attack.
A, Angiogram of aortic arch demonstrates a common origin of the left common carotid artery with the right brachiocephalic artery. There is
a short segment 75% stenosis (arrow) involving the proximal brachiocephalic artery immediately distal to the origin of the left common
carotid artery. B, Angiogram via the introducer sheath confirms stenosis of proximal right brachiocephalic (arrow). C, Angiogram via the
introducer sheath following angioplasty and balloon-expandable stent (9 mm) placement (arrow) shows an excellent radiographic result.
To avoid theoretical embolic complications from stent protrusion into the carotid artery, the stent was placed at the origin of the right
brachiocephalic artery without extending into the left common carotid artery. This was not ideal in that the atherosclerotic disease extended
by angiography to the origin of the brachiocephalic artery and could predispose to restenosis at the brachiocephalic origin.
the contralateral vertebral artery is stolen from the dizziness or ataxia. Angioplasty and stenting have
posterior fossa via the basilar artery then coursing down achieved widespread acceptance as the procedure of
the ipsilateral vertebral artery to supply the arm. How- choice in this situation. Technical success exceeds 95%
ever, simple reversal of blood flow in a vertebral artery for stenotic lesions; for total obstructions, success rates
has been found in 6% of patients undergoing carotid fall to 65% to 85%, largely from failure to traverse the
ultrasound, far more often on the left than the right side occlusion.15-17 The 5-year clinical patency rates range
(82%).28 The diagnosis of subclavian steal syndrome is between 82% and 89%.29,30 Protection devices are rarely
reserved for patients who are symptomatic from result- used in the vertebral artery during subclavian artery
ing posterior fossa ischemia, typically complaining of angioplasty and stenting based on the concept that the
A B
20. NEUROINTERVENTIONS 609
brain is protected from microemboli by the flow reversal group had strokes referable to the vertebral artery
in the ipsilateral vertebral artery.31 Nonetheless, strokes distribution. A Cochrane database review in 2005
have been reported.30 Stenting across the vertebral artery identified 173 reports of vertebral artery stenting and
origin has been undertaken, particularly when symp- found a 30-day major stroke and death rate of 3.2%
toms consist of arm claudication and the ipsilateral and a 30-day transient ischemia and nondisabling
vertebral artery is the nondominant vertebral vessel. stroke rate of 3.2%.34
Cervical vertebral artery atherosclerotic disease is The published results for angioplasty and stenting of
prevalent in patients with peripheral arterial disease. the carotid artery bifurcation are mixed.19,35-39 Table 20-2
However, the diagnosis is often difficult owing to the presents the six clinical trials in which carotid artery
relative vagueness of symptoms. It may even be dif- stenting (CAS) was randomized to carotid endarterec-
ficult to determine whether patient complaints are tomy (CEA).19,35-39 The studies varied widely in terms of
related to a vertebral artery stenosis or occlusion if the inclusion criteria, symptoms, endpoints, qualifications of
contralateral vertebral artery is patent or the ipsilat- the operators, and standardization of techniques. Out of
eral collateral circulation is abundant. Once a connec- five studies, three found that CAS was not inferior to
tion is made between symptoms and vertebral artery CEA while two found CAS inferior. Thus far, the best
obstruction, angioplasty itself is straightforward and study comparing CAS with CEA in surgically suitable
produces acceptable results. Angioplasty with stent patients is the Carotid Revascularization Endarterec-
placement is performed for lesions at the orifice of the tomy versus Stenting Trial (CREST) published in 2010.35
vertebral artery but angioplasty alone may be other- This randomized trial included 2502 patients, both symp-
wise applied through the extracranial vertebral artery tomatic and asymptomatic, followed for a median of
(Fig. 20-5). Procedural and clinical success has been 2 years after treatment for the primary endpoints of
reported to be 100% and 90.5%, respectively, with stroke, myocardial infarction, and death. There was over-
79.3% of individuals remaining symptom-free at all no difference between the two groups. However, in the
1 year.32 Only one small randomized study of verte- 30-day periprocedural period, stroke occurred more often
bral artery angioplasty has been carried out, which in the stenting group (CEA 2.3% vs. CAS 4.1%) whereas
included 16 patients with vertebral artery disease, myocardial infarction was greater in the surgery group
eight treated with medical therapy and eight by endo- (2.3% vs. 1.1%) (see Table 20-2). The estimated 4-year rates
vascular stenting.33 At a mean of nearly 5 years, neither for the primary endpoints were equivalent.
A B
610 V. MISCELLANEOUS VASCULAR INTERVENTIONS
TABLE 20-2 Comparison of Studies Randomizing Surgical Carotid Endarterectomy to Carotid Artery Stenting
CAVATAS, Carotid and Vertebral Artery Transluminal Angioplasty Study; CAS, carotid artery stenting; CEA, carotid endarterectomy; CREST, Carotid Revascularization
Endarterectomy versus Stenting Trial; DPD, distal protection device; EVA-3S, Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis
trial; ICSS, International Carotid Stenting Study; MI, myocardial infarction; SAPPHIRE, Stenting and Angioplasty with Protection in Patients at High Risk for
Endarterectomy trial; SPACE, Stent-Supported Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy trial.
related to chronic ischemia rather than cerebral embo- associated with significantly higher rates of adverse
lism. Complete recovery is the rule in mild cases, but events and provided no benefit over aspirin.48 Anti-
disability and death can occur in more severe cases. platelet agents, including aspirin and clopidogrel, are
currently the primary drugs used in the medical treat-
ment of intracranial atherosclerotic disease.
INTRACRANIAL
ATHEROSCLEROTIC DISEASE Endovascular Therapy
Endovascular therapy for intracranial atherosclerosis
has been limited to symptomatic patients with greater
Natural History than 50% stenosis who have failed medical therapy
Atherosclerosis of the major intracranial arteries ac- and asymptomatic patients with stenoses who are coun-
counts for an estimated 8% to 10% of ischemic strokes in seled regarding the therapeutic options and a wish to
the United States.43 Furthermore, among patients with a proceed with recanalization.49 To lessen the likelihood
70% to 99% stenosis and symptoms (transient ischemic of vessel perforation, intracranial endovascular therapy
attacks or stroke), a second ischemic event occurs within should be limited to the major proximal vessels (intra-
1 year in the territory of the symptomatic artery in 11% cranial carotid and vertebral, basilar, M1, and rarely P1;
of individuals.44 Although the actual prevalence of intra- see Fig. 20-1). Autopsy data have noted that the distri-
cranial atherosclerotic disease is largely unknown, it is bution of intracranial atherosclerotic disease largely in-
more common in African Americans and Hispanics, as volves these same vessels.50
well as patients with insulin-resistant diabetes and those Intracranial angioplasty procedures are typically
with hypercholesterolemia and inflammation.45,46 (though not universally) performed with general anes-
thesia. The therapeutic options are angioplasty alone or
Treatment angioplasty with stenting. It is usually easier to negoti-
ate the tortuous vertebral and carotid vessels with a bal-
Medical and Surgical Therapy loon alone; advancing a stent through these pathways
Surgery for intracranial atherosclerosis was evaluated in can be quite difficult. Stenting has thus far not been
the 1985 external carotid to internal carotid bypass shown to be superior to angioplasty alone and are thus
study, which concluded that bypass failed to reduce the usually grouped together in publications.51 Angioplasty
risk of ischemic stroke compared with medical therapy.47 alone carries the fears of an intimal dissection, some
Although interest has revived recently, surgery is largely advocating that the occurrence of a significant intimal
reserved for patients who have failed medical therapy flap can be limited by slow, prolonged balloon inflations
and who are not candidates for or have failed endovas- (approximately 2 minutes) as opposed to quick, sudden
cular interventions. inflations.52 Stents can be either of the self-expanding
Based for the most part on the failure of surgical by- or balloon-expandable variety (Figs. 20-6 and 20-7).
pass, medical therapy for intracranial atherosclerosis Balloon-expandable stents are for the most part coro-
has focused on the use of warfarin. However, the results nary stents used in an off-label fashion. A single self-
of the Warfarin-Aspirin Symptomatic Intracranial Dis- expanding stent (Wingspan Stent System, Boston Scientific,
ease study (WASID) demonstrated that warfarin was Natick, Mass.) has a human device exemption from the
A B
U.S. Food and Drug Administration (FDA) for intracra- compared medical to endovascular therapy in symp-
nial use (see Fig. 20-6). tomatic patients with a 70% to 99% stenosis of a major
Data regarding intracranial angioplasty and stenting intracranial artery. The study was recently stopped due
are now being published.53 A systematic outcomes review to a high rate of complications in the stenting group.
in 2009 identified 31 studies reporting on 1177 proce- Publication of the data is pending at this writing.
dures, performed mostly (98%) in symptomatic patients Complications of intracranial angioplasty include
with high-grade (mean 79%) intracranial stenoses.54 There stroke from intimal dissection or distal embolization.
was a high technical success rate (median 96%) with peri- Intracranial arteries are very thin-walled structures. Vessel
procedural minor or major stroke and death rates ranging perforation is a particular risk of angioplasty at these
from 0% to 50% (median 7.7%). Periprocedural complica- sites with increasing likelihood at more distal locations.
tions were significantly higher in the posterior versus the Careful guidewire placement during lesion traversal is
anterior circulation, but did not differ between patients essential, taking care to avoid migration of the wire tip
treated with balloon-mounted versus self-expanding into small vessels. Balloon and stent sizing must be
stents. However, restenosis greater than 50% at a mean of carefully calculated to avoid overdistention of the artery
8.7 months occurred more frequently after the use of self- during angioplasty. There is little chance for rescue of an
expanding stents. acutely perforated intracranial vessel.
Two multicenter prospective nonrandomized patient
registries have been conducted by product manufac-
turers resulting in human device exemption status from ACUTE STROKE
the FDA: the Stenting of Symptomatic Atherosclerotic
Lesions in the Vertebral or Intracranial Artery (SSYLVIA)
Etiology and Natural History
study and the Wingspan stent system with Gateway PTA
Dilation Catheter (Boston Scientific, Fremont, Calif.).55,56 By definition, stroke refers to a fixed neurologic deficit
The SSYLVIA trial used the Neurolink System, a self- of greater than 24 hours duration. The estimated inci-
expanding stent (then Guidant, Menlo Park, Calif.), and dence of stroke in the United States is approximately
found an overall symptomatic restenosis rate of 13.7% 795,000 per year. Stroke is the third leading cause of
with an initial procedural success rate of 85.5%.55 The death in the United States and the leading cause of long-
Wingspan study had a procedural success rate of 98%, term disability.57 Eighty-three percent of strokes are
although a 7.5% greater than 50% restenosis rate at ischemic and related to large artery atherosclerosis, throm-
6 months.56 The Wingspan self-expanding stent is avail- boembolism, small vessel occlusion, or other causes.58
able under a human device exemption; the Neurolink The remaining 17% of cases are hemorrhagic (about 10%
stent is not currently available. A randomized study intracerebral and 7% subarachnoid).
between the Wingspan stent and best medical therapy Stroke is the clinical situation that follows neurologic
was undertaken in the Stenting and Aggressive Medical cell death because of decreased blood flow. However, acute
Management for Preventing Recurrent Stroke and Intra- stroke has a large component of fluctuating ischemia. The
cranial Stenosis trial (SAMMPRIS). This large study ischemic penumbra refers to the region of threatened tissue
20. NEUROINTERVENTIONS 613
adjacent to the core of evolving infarction. It is thought therapy is determined (Box 20-2). A key item in the his-
that this area has a limited and variable interval of viabil- tory is the exact time of symptom onset (or time the pa-
ity and is potentially salvageable by the quick restoration tient was last known to be in his usual state of health).
of blood flow. The primary goal of acute stroke treatment The physical examination should determine vital
is preventing frank infarction in this fragile region. signs, the National Institutes of Health Stroke Scale
(NIHSS), and likely vascular territory and etiology of
stroke if possible. The NIHSS evaluates neurologic im-
Clinical Features pairment on a scale of 1 to 42, with higher scores (21 to
The patient should be expediently evaluated by the 42) indicating severe neurologic impairment (www.
neurologic stroke team for findings of ischemic stroke ninds.gov/disorders/stroke/strokescales). Laboratory
(Fig. 20-8). A complete history is obtained, sometimes studies should include coagulation parameters and
from a family member. The presence of contraindica- blood glucose levels, because profound hypoglycemia
tions to the administration of intravenous thrombolytic or hyperglycemia can mimic stroke.
Imaging
Noncontrast CT
CTA
CT perfusion
Hemorrhage No hemorrhage
Ischemic change >1/3 Ischemic change <1/3
vascular territory vascular territory
No thrombus to first or Thrombus up to first or
second order second order
Nonsalvageable tissue Salvageable tissue by
by perfusion perfusion
No intraarterial
intervention
FIGURE 20-8 Flow chart of the workup of stroke. Evaluation and treatment flow diagram for patients presenting with acute stroke
symptoms.
614 V. MISCELLANEOUS VASCULAR INTERVENTIONS
BOX 20-2
I N T R AV E N O U S R E C O M B I N A N T T I S S U E P L A S M I N O G E N
A C T I VA T O R F O R A C U T E I S C H E M I C S T R O K E *
*From package insert for alteplase (Acitvase; Genetech, Inc., South San Francisco, Calif.).
Only the time from symptom onset for the administration of intravenous t-PA is greatly different than the intraarterial administration.
20. NEUROINTERVENTIONS 615
A B C
D E
FIGURE 20-9 Thrombolysis of acute stroke in a 16-year-old male patient with acute onset of dense left hemiparesis approximately 4 hours
before the procedure. A, Noncontrast computed tomography (CT) demonstrates dense left middle cerebral artery (arrow). B, CT angiography
demonstrates thrombus within the right M1 segment (arrow) with preservation of distal perfusion to into branches. C, Right internal carotid
angiogram and anterior posterior projection demonstrates occlusion of the right middle cerebral artery (arrow) with pial collaterals from the
anterior cerebral artery (arrowheads). D, Angiogram after microcatheter (arrow) has been placed into thrombus and infusion of rtPA has begun.
There is now some antegrade flow within the middle cerebral artery (arrowhead). E, Final angiogram following the infusion of 25 mg of rtPA
into the right middle cerebral artery. There is antegrade flow in the vessel with an excellent radiographic result.
616 V. MISCELLANEOUS VASCULAR INTERVENTIONS
Endovascular Therapy
decision-making is still lacking. MR imaging (MRI) has
many features that make it attractive as an initial im- PATIENT SELECTION
aging tool, but it is often too time-consuming to obtain If IV t-PA administration is not an option, endovascular
in the acute setting. intervention should be considered. Recanalization can
be accomplished by chemical thrombolysis with IA infu-
Treatment sion of a thrombolytic agent, mechanical thrombectomy,
or both.
Medical Therapy Because the fibrinolytic agent is delivered directly
The cornerstone of modern medical therapy for acute into the thrombus, the effective dose is much lower than
stroke is administration of intravenous (IV) recombi- with systemic administration. Based on animal studies
nant tissue plasminogen activator (t-PA) (see Fig. 20-8). and limited human data, a therapeutic window of 6 hours
The standard protocol for t-PA administration is based for reperfusion of anterior cerebral (carotid distribution)
on the pivotal National Institute of Neurological Disor- ischemia with IA delivery is the threshold used by most
ders and Stroke (NINDS) study published in 1995, stroke centers. This 6-hour limit has been chosen as a
which compared IV t-PA with placebo administered realistic time interval that will maximize both patient
within 3 hours of the onset of stroke symptoms.59 This safety and chances of success.
trial found a statistically significant reduction in the Without direct treatment, outcomes for vertebro-
degree of long-term disability for the group treated basilar stroke are often dismal, with an 80% rate of
with IV t-PA. Importantly, although there were more death or significant disability.61,62 Stroke in this circula-
symptomatic hemorrhages in the t-PA group, the ben- tion is less likely to be thromboembolic in nature and
efit from thrombolytic therapy was not offset with is more often associated with intracranial atheroscle-
any increase in mortality. The biggest obstacle for the rotic disease.63 As such, angioplasty and sometimes
administration of IV t-PA is timing. Many patients do stent placement is often necessary after thrombolysis
not arrive at the hospital within 3 hours of symptom (Fig. 20-10). For that reason as well as a lessened rate
onset, and even when they do, a comprehensive effort of hemorrhagic complications following IA thrombol-
is required to evaluate a patient, make a treatment deci- ysis in the posterior circulation, the window for the
sion, and then expediently administer t-PA. Practically administration of thrombolytic agents is usually in-
speaking, a patient must present to the hospital well creased to 12 hours from symptom onset.64
before 3 hours of symptom onset to qualify for IV t-PA As with thrombolysis in the peripheral system, there
treatment. Recent studies, most notably the European are controversies regarding protocols (drug, dose, in-
Cooperative Acute Stroke Study, suggest that the thera- fusion duration) for the application of IA thrombo-
peutic window for safe, effective intravenous throm- lytic agents in acute stroke. In the United States, the
bolysis in acute stroke may be extended up to 4.5 hours most commonly used agent is t-PA, although much of
following symptom onset, albeit in a very select patient the data are based on prior reported experience with
population.60 urokinase.64,65 Although there is widespread agreement
A B C
FIGURE 20-10 Basilar thrombolysis and angioplasty with stent placement in a 56-year-old man who was admitted to the stroke service
with evidence of posterior fossa ischemia. The patients neurologic examination acutely deteriorated. A, Right vertebral artery angiogram
shows complete occlusion of the proximal basilar artery (arrow). B, Following thrombolysis, residual stenosis (arrow) was noted, which
reoccluded and was again opened with additional recombinant tissue plasminogen activator (total dose 10 mg). C, Angioplasty and stenting
with a 3- # 9-mm coronary stent produced an excellent radiographic result (arrow).
20. NEUROINTERVENTIONS 617
on which patients are eligible for IV t-PA, the indi- injected (see Fig. 20-9). Multiple injections can be per-
cations for IA therapy vary from institution to institu- formed until the thrombus is dissolved, a predetermined
tion and even among interventionists within the same maximum dose of agent is administered, or a predeter-
institution. Some practitioners reserve IA therapy for mined time allotted for revascularization expires. Doses
patients not eligible for IV therapy; others routinely for t-PA vary among interventionists but it is typically
give eligible patients lower bridging doses of IV t-PA injected in small increments (1 to 5 mg) with frequent
to transition to IA therapy; still others proceed with IA angiography to assess for recanalization. Predetermined
therapy even after full-dose IV t-PA has been given in maximum doses vary among operators but were re-
clinically refractory patients. ported in a safety and efficacy analysis to range from
20 to 60 mg.66
Technique Mechanical thrombus disruption or removal is consid-
Although subject to some controversy, stroke interven- ered when chemical thrombolysis is failing or as a thera-
tions are probably best performed under the more con- peutic option when the patient presents too late from
trolled conditions of general anesthesia. The use of symptom onset to be considered for IA thrombolysis (see
heparin in stroke thrombolysis is controversial, because Fig. 20-8). Although the time frame varies considerably,
there is an increased risk of intracranial hemorrhage.64 a window of up to 8 hours in the anterior circulation and
Diagnostic angiography is performed initially to evalu- 24 hours in the posterior circulation is used for mechani-
ate areas of occlusion and degree of collateral flow, and cal thrombus removal. However, few data are available to
as a map for thrombolytic therapy. Through a 6-Fr guid- substantiate these intervals. Several specialized mechani-
ing catheter, a microcatheter is placed either against or cal thrombus removal systems are approved by the FDA
into the thrombus, and the thrombolytic agent is slowly for intracerebral use (Fig. 20-11). The Merci mechanical
A B C
D
FIGURE 20-11 Mechanical thrombus disruption and removal in a 62-year-old man who recently underwent coronary bypass surgery
and during his postoperative course became acutely hemiplegic on the right side and aphasic. A, Lateral angiogram of the left internal carotid
artery demonstrates occlusion of the internal carotid artery (arrow) just above the take-off of the posterior communicating artery (arrowhead).
Following the administration of 20 mg of recombinant tissue plasminogen activator (t-PA) in divided doses, forward flow could not be estab-
lished in the distal internal carotid artery. B, The Penumbra stroke system was placed into the distal internal carotid artery and middle cerebral
arteries (arrow). C, Image of Penumbra System demonstrating catheter and separation (arrow). D, Postangiogram of the left internal carotid
artery demonstrates flow in the distal internal carotid artery and into the middle cerebral artery and anterior (A1) artery. There is occlusion
of the left A2 vessel (arrow), and a microcatheter was placed in this location and additional t-PA was given but this did not open. E, Merci
Retriever demonstrating the platinum wire as well as suture material that served to remove thrombus. (C, Courtesy of Penumbra, Alameda, Calif.,
with permission. E, Courtesy of Concentric Medial, Mountain View, Calif., with permission.)
618 V. MISCELLANEOUS VASCULAR INTERVENTIONS
thrombolysis device (Concentric Medical, Mountain View, the retriever alone was achieved in 43% of patients
Calif.) consists of a microwire and suture which grasps and with additional IA t-PA in 64%.70 The Mechanical Em-
the thrombus for removal via a large lumen balloon cath- bolus Removal in Cerebral Ischemia (MERCI) trial, which
eter (see Fig. 20-11E). The device and the microcatheter was a prospective single-arm trial of 164 patients, demon-
are withdrawn together through the balloon catheter to strated recanalization in 55% of the vessels with the device
remove intact clot. The Penumbra Stroke System (Penum- alone. The initial Penumbra trial consisted of 20 patients
bra, Alameda, Calif.) consists of a specialized microcathe- treated within 8 hours of symptom onset and produced
ter with a distal tip that separates from the catheter lumen recanalization in all treated cases.71 This study was fol-
(see Fig. 20-11C). Thrombus is then removed using con- lowed by a larger prospective single-arm multicenter trial
trolled suction provided by a specialized pump. (the Penumbra Stroke Trial) conducted at 24 international
centers that enrolled 125 patients and found partial or
Results complete recanalization in 82% of patients.72
Despite relatively widespread use, evidence for the value
of endovascular treatment of acute stroke consists of Complications
small series, case reports, and manufacturer sponsored The most dreaded complication of endovascular stroke
studies.67 The best published study to date is the Prolyse therapy is significant intracranial bleeding, which occurs
in Acute Cerebral Thromboembolism trial (PROACT ).64 in about 15% of cases.64 Keep in mind, to some degree
In this investigation, patients with middle cerebral artery hemorrhage is part of the evolution of stroke, occurring
thrombus were randomized to receive recombinant pro- in 43% of patients absent any intervention and is de-
urokinase (rproUK), a nonFDA-approved agent similar pendent upon a number of factors including degree of
to urokinase or heparin. In the initial phase of the trial neurologic deficit, size of the infarct, and an embolic
(often termed PROACT I), 26 patients were treated with etiology.73 Intraprocedure hemorrhage is suggested by
rproUK and 14 with placebo. Both recanalization and sudden hemodynamic fluctuation due to increased intra-
intracranial hemorrhage were greater in the rproUK cranial pressure and proven by extravasation of contrast
group. All patients in the rproUK group who had hemor- on the cerebral angiogram. Alternatively, newer flat panel
rhage had early CT changes (five patients) of greater than angiographic systems allow for CT scanning of sufficient
33% of the middle cerebral artery territory. Such a pattern quality to detect hemorrhage. If bleeding is suspected,
on CT has become a relative contraindication for throm- thrombolytic infusion should be discontinued immedi-
bolysis. It was also noted that hemorrhage was associ- ately and anticoagulation reversed.
ated with higher heparin doses. The second phase of the
study (often termed PROACT II) enrolled 180 patients
who received either rproUK plus low-dose heparin or PREOPERATIVE TUMOR
low-dose heparin alone.64 The results of this study EMBOLIZATION
showed long-term benefit (slight or no neurologic im-
pairment) in 40% of patients in the thrombolysis group
Etiology and Clinical Features
versus 25% with the heparin group.
Another randomized study, the Middle Cerebral Meningiomas are thought to arise from arachnoidal cap
Artery Embolism Local Fibrinolytic Intervention Trial cells, which reside in the arachnoid layer covering
(MELT) randomized 114 patients to receive urokinase the surface of the brain and thus may arise in a variety
versus heparin alone.65 The results showed improved of locations.74 They may be entirely asymptomatic or
functional outcomes in the thrombolysis group compared present with headaches or neurologic deficits. In the
with controls. The study, however, was discontinued head and neck region, the normal paraganglia are asso-
upon the approval of IV t-PA in Japan. No randomized ciated with the parasympathetic nervous system and
trials have been completed for posterior circulation IA paragangliomas arise from these parasympathetic sites.75
thrombolytic therapy. The one study that was initiated Patients with cervical paragangliomas typically develop
was terminated due to slow recruitment of patients and a painless, slowly enlarging mass in the lateral aspect
ultimately the removal of urokinase from the market.68 of the neck. Tinnitus and hearing loss are earliest symp-
Metaanalyses of existing reports that encompassed 344 toms of tympanicum and jugulare tumors. The patho-
patients treated with IA thrombolysis found death or physiology of juvenile angiofibromas is incompletely
neurologic dependency in 76%, essentially equal to those understood with various theories as to even its site of
receiving IV t-PA. There were, however, better recanali- origin including originating from nonchromaffin para-
zation rates with IA administration.69 ganglionic cells of the terminal branches of the maxillary
Data on mechanical removal devices is principally artery, accounting for their dense hypervascularity and
based on manufacturer-sponsored publications. The arterial supply.76 Juvenile nasopharyngeal angiofibroma
Merci device was initially studied in a 30-patient phase I presents clinically as a nasal mass and, when symptom-
multicenter trial, in which successful recanalization with atic, usually causes epistaxis.
20. NEUROINTERVENTIONS 619
TABLE 20-3 Arterial Supply from the External Carotid Artery to Tumors and Epistaxis
Meningioma MMA (most common) Particles !150 $m if microcatheter tip close to tumor;
Accessory MA branches otherwise particles 250 $m and larger
IMax-ethmoidal branches
Occipital artery (tumor posterior)
STA (tumor superior/falcine)
Paraganglioma
Cervical carotid body/vagal Ascending pharyngeal Particles !150 $m if microcatheter tip close to tumor;
Facial otherwise particles 250 $m and larger, especially if
Thyroidal A-V shunting
Lingual
Temporal jugular/tympanic Ascending pharyngeal Particles !150 $m if microcatheter tip close to tumor;
Distal internal maxillary otherwise particles 250 $m and larger, especially if
Posterior auricular A-V shunting
Occipital
Juvenile angiofibroma and Distal internal maxillary Particles "250 $m, even larger if bilateral supply being
epistaxis Facial embolized
Especially worrisome for skin necrosis
Important to assess venous anatomy, particularly relative to the dural sinus for meningioma and the jugular veins for paragangliomas,
which will affect the surgical approach.
Many of these may also have supply from vertebral and intracranial arteries. For juvenile angiofibroma, arterial supply may vary
significantly if prior surgery has been undertaken.
Smith TP. Embolization in the external carotid artery. J Vas Interv Radiol 2006;17:1897.
IMax, internal maxillary; MA, meningeal artery; MMA, middle meningeal artery; STA, superficial temporal artery.
620 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B C
FIGURE 20-12 Embolization of meningioma. A 72-year-old male with large right sphenoid meningioma for preoperative embolization.
A, Injection of the internal maxillary artery demonstrates supply to the meningioma mostly from the middle meningeal artery (arrow) and an
accessory meningeal artery (arrowhead). Note the sunburst pattern of the meningioma. B, Following particle embolization of both meningeal
arteries, there is an excellent radiographic result. Only a small amount of tumor blush is noted from a small posterior meningeal supply
(arrow). C, Lateral view of angiogram after particle embolization of the middle meningeal artery in a different patient with a meningioma
(arrowheads). Note the prominent choroidal blush (arrows) demonstrating supply to the orbital contents. Embolization of this vessel runs a
very high risk of causing ipsilateral blindness. Angiography of the middle meningeal artery should always include the orbit on at least one
lateral view to rule out the presence of the choroidal blush. (From Smith TP. Embolization in the external carotid artery. J Vas Interv Radiol
2006;17:1897, with permission.)
between 7 and 9 days following embolization.80,81 There collateral blood supply (see Table 20-1). Postembolization
was no significant correlation between interval from hemorrhage is reported in up to 5% of patients.79
embolotherapy and operative blood loss or procedure- Given the relative paucity of data supporting the
related complications.81 Therefore the interventionalist technique, most experts recommend preoperative me-
can perform the embolization procedure at any time ningioma embolization only for highly vascular tumors
within 7 days of surgery and still achieve the desired as assessed by cross-sectional imaging, in particular
results. those at the skull base.77 In surgery at the cranial base,
Since its first description in 1973, preoperative embo- the feeding vessel is often not approachable operatively
lization for meningiomas has been controversial.82 It is until the majority of the tumor has been resected. In this
not clear whether the procedure actually reduces opera- situation, preoperative embolization is thought to be
tive blood loss sufficiently to outweigh the potential for highly useful.
complications. Some historical series describe decreased
blood loss and reduced number of blood transfusions Paragangliomas
with preoperative embolization.83 Unfortunately, no ran- Paragangliomas of the head and neck are neoplasms
domized trials are available to properly answer the derived from neural crest cells and occur along the
question. paraganglion pathway.85 They are typically at four lo-
Major complications from meningioma embolization cations from which they derive their names: carotid
include neurologic deficits and tumor hemorrhage. Neu- body tumors, jugular bulb (jugulare), tympanic plexus
rologic deficits (including cranial nerve palsy, blindness (tympanicum), and vagal nerve (vagale). The carotid body
and stroke) occur in up to 3% of patients.84 The most tumor is the most common and characteristic due to its
feared cranial nerve palsy is attributed to the facial gan- splaying of the common carotid bifurcation (Fig. 20-13).
glia after middle meningeal artery (MMA) embolization Paragangliomas are notoriously hypervascular lesions
proximal to the facial canal. Blindness most often origi- and may be multifocal in up to 22% of patients.86 Diagnos-
nates from MMA embolization when a meningolacrimal tic angiography of these tumors should include ICA injec-
variant supplying the ophthalmic/central retinal artery is tion with venous phase imaging. Venous phase imaging is
not recognized (see Fig. 20-12C). Stroke can occur when particularly important with jugulare tumors to assess the
there is a failure to recognize extracranial to intracranial extent of intravenous involvement. ICA angiography is
20. NEUROINTERVENTIONS 621
A B
A B
reserving open surgical ligation of the sphenopalatine ECA (in particular its small labial branch) or the
and ethmoidal arteries for when other measures fail. anterior and posterior ethmoidal branches of the oph-
thalmic artery arising from the ICA.
Endovascular Therapy Complete diagnostic angiography is essential in
Less than 1% of patients presenting with epistaxis require the evaluation of the patient with epistaxis. Full ECA
embolization or surgery.104 Embolotherapy should be con- angiography is imperative as bleeding can originate
sidered for intractable epistaxis that is refractory to several from unsuspected sites such as the accessory meningeal
trials of nasal packing and endoscopic therapy. Emboliza- artery.105 In addition, angiography may demonstrate the
tion is an excellent therapeutic choice for posterior epi- etiology for bleeding (e.g., tumor blush, vascular malfor-
staxis, and in some centers takes an early and prominent mation, traumatic pseudoaneurysm.) The ECA gives rise
role in its treatment. The choice between surgery and em- to important extracranial to intracranial collaterals, par-
bolotherapy is often based on local expertise. ticularly when the ICA is occluded (Fig. 20-16). Visualiza-
The anatomy of the arteries usually responsible for tion of the ICA distribution is therefore critical, not only
epistaxis is complex and involves both external and to identify occlusions with reconstitution from ECA col-
internal carotid artery branches. The sphenopalatine laterals but also because epistaxis may be caused by ICA
and greater palatine branches from the internal maxillary disease itself (e.g., aneurysms.) During angiography, the
artery are the usual sources (Fig. 20-15). Less often, actual bleeding site is rarely visualized particularly in
bleeding occurs from the facial artery branch of the idiopathic epistaxis and when nasal packing is in place.
A B C
FIGURE 20-15 Epistaxis embolization in a 74-year-old woman with history of persistent left
epistaxis. A, Left common carotid angiogram in the frontal view demonstrates a normal internal
carotid artery and a nasal mucosal blush from the external carotid artery (arrow). B, Angiogram via
the microcatheter of the distal internal maxillary/sphenopalatine artery (arrow) showing intense
nasal mucosal blush (arrowheads). C, Postembolization angiogram via the microcatheter of the distal
internal maxillary/sphenopalatine artery (arrow) showing significant decrease in the nasal mucosal
blush (arrowhead). D, Lateral view of the alar branch (arrow) of left facial artery showing supply to
the nasal mucosa. If epistaxis is confined to the left side, this artery should be embolized as well.
D
624 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B
FIGURE 20-16 Lateral view of a common carotid injection in which the internal carotid artery is occluded. A, Early intracranial views
demonstrate filling of the ophthalmic artery (arrows) via ethmoidal collaterals (arrowheads). Flow in the ophthalmic artery is retrograde and fills
the internal carotid artery (gray arrow). B, Later view demonstrates complete filling of the intracranial internal carotid artery supply via retrograde
flow from the ophthalmic artery. (From Smith TP. Embolization in the external carotid artery. J Vas Interv Radiol 2006;17:1900, with permission.)
Embolization is most often performed via a guiding some disagreement as to the utility of embolotherapy for
catheter (usually 6 Fr) placed in the proximal ECA with a epistaxis. Direct comparison of surgery and transcatheter
microcatheter advanced into the vessel to be embolized, embolization in a randomized prospective form has not
usually the internal maxillary artery. The most popular been undertaken. Santaolalla and colleagues107 retrospec-
embolic agent is PVA, 150 to 250 $m in diameter, but size tively reviewed 28 patients with intractable posterior epi-
ranges from 50 to 750 $m have been used.6 Proximal em- staxis treated by embolization and 28 unembolized con-
bolic agents (coils) have been used safely and effectively trol patients and found no significant differences in
for treatment of epistaxis but are not generally recom- outcomes between the two groups.
mended because rebleeding may occur from collateral
circulation that develops beyond the occluded site.
If no bleeding or abnormality is seen, empirical emboli- HEAD AND NECK TRAUMA
zation may be indicated. As a rule, the bilateral internal
maxillary arteries are treated when the side of hemorrhage
is clinically unknown, or the ipsilateral internal maxillary
Etiology and Clinical Features
artery and facial artery are treated when the side of hemor- The mechanisms for neurovascular arterial trauma in-
rhage is known (see Table 20-3). In general, at least one in- clude criminal or accidental blunt or penetrating injuries,
ternal maxillary artery is embolized in virtually all patients iatrogenic causes (e.g., surgery, biopsy, endovascular pro-
and the facial artery in about 27% to 48% of patients.6 Em- cedures, central venous line placement), and radiation
bolization of the facial artery must be performed with great therapy. The head and neck has an extensive vascular
care, particularly with respect to particle size. Particles supply, which is advantageous for endovascular treat-
should lodge distal enough to control hemorrhage yet ment because the rich collateral network helps prevent
proximal enough to preserve the distal supply of the termi- postembolic ischemic injury. The common and internal
nal alar artery supplying the skin of the nasal ala. carotid arteries are closely associated with the jugular
Smith6 reviewed the literature for epistaxis emboliza- veins, and the vertebral arteries are surrounded by an
tion from 1994 to 2006 and since that time three additional extensive venous network. Therefore injury to the carotid
studies have been reported.106-108 Series size ranged from or vertebral artery with concomitant venous injury pre-
12 to 107 patients. Primary success rates averaged 87% disposes to arteriovenous fistula formation.
and ranged from 75% to 100% with recurrence rates, When symptomatic, patients present with external
following successful embolization, ranging up to 25%. bleeding, an expanding or pulsatile mass, or neurologic
There were 23 (3%) major complications consisting of symptoms. When asymptomatic, vascular injury is usu-
15 strokes, two cases of monocular blindness, four cases ally detected on imaging studies obtained to identify
of skin sloughing, one asymptomatic ICA dissection, and bony or parenchymal trauma.
one postprocedure myocardial infarction. In addition,
patients often complained of facial pain and numbness
and a degree of trismus, all self-limited. Fukutsuji and
Imaging
coworkers106 described minor complications consisting Whereas sonography can delineate some vascular abnor-
of local pain, headache, numbness or edema occurring in malities in the neck (e.g., intimal dissections of the carotid
13 of 22 (59%) patients; however, none of these symptoms arteries, arteriovenous fistulas, major vessel occlusions),
persisted for more than 1 week. Interestingly, there is still its primary role is evaluation of very unstable patients
20. NEUROINTERVENTIONS 625
who cannot be readily moved. CT (including CT angiog- Zone 2, from the thoracic outlet to the angle
raphy) is the principal imaging modality for head and of the mandible
neck trauma. It provides excellent images of the bony Zone 3, superior to the angle of the mandible
structures, including the face, cranium, and spine, and
can readily delineate arterial injuries. Catheter angiogra- Classically, zone 2 lesions are managed with surgical
phy is usually reserved for patients who are clinically repair although endovascular means have also been ap-
unstable and have a high clinical suspicion for an arterial plied. Zones 1 and 3 are most often approached by en-
injury, for difficulty with diagnosis, or as a prerequisite to dovascular techniques. Injuries to branches of the ECA
intervention. In evaluating the trauma patient, complete, are not easily reached by surgical exposure and are
four vessel angiography is recommended if the pa- better treated by endovascular means.109 Surgical liga-
tients clinical situation allows. This study includes both tion of the proximal ECA trunk is not usually performed
carotids and both vertebral arteries, and demonstrates the in deference to endovascular therapy.
suspected areas of abnormality, while also excluding
other areas of injury and defining potential collateral sup- Endovascular Therapy
ply if vessel sacrifice (occlusion) should become neces- Intimal dissection may occur spontaneously, from blunt
sary. The typical angiographic findings are vasospasm, or penetrating trauma, or catheterization procedures.
intimal disruption or dissection, extravasation, pseudoa- Dissection is most worrisome in the extracranial carotid
neurysm, arteriovenous fistula, and vessel occlusion. and vertebral arteries due to the possible associated
neurologic ischemic events. Treatment of these dissec-
Treatment tions must be highly individualized to a particular pa-
tient and their symptoms. Patients with extensive trau-
Surgical Therapy matic injuries cannot be systemically anticoagulated
Based on the ease and suitability for surgical repair, particularly for long intervals; medical therapy alone is
carotid artery injuries are categorized by location: often a poor option. Endovascular stenting using either
bare metal or covered devices has been shown in small
Zone 1, from the origins of the great vessels series to be quite effective in these patients, even for
inferiorly to the thoracic outlet complete occlusions82 (Fig. 20-17). In a recent literature
A B
626 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B C
FIGURE 20-18 Test occlusion and carotid artery occlusion in a 56-year-old man with a history of recurrent vocal cord squamous cell
carcinoma that involves the right internal carotid artery. He is scheduled for additional surgery that may include carotid artery resection.
For preoperative test occlusion and endovascular carotid artery occlusion. A, Right common carotid angiogram demonstrates narrowing
of the distal common and proximal internal carotid artery (arrow) with occlusion of the external carotid artery. B, Occlusion balloon (arrow)
placed in proximal common carotid artery for 20 minutes. Neurologic examination was normal. Patient also had a normal single photon
emission computed tomogram following clinical test occlusion, whose results were normal. C, Internal carotid artery was occluded in the high
cervical region using coils (arrow). Carotid artery shows no flow after occlusion (arrowhead). Carotid artery was occluded distally at the request
of the referring surgeon.
carotid artery occlusion can be based solely on the de- life- threatening hemorrhage (about 50% and 60%, respec-
gree of collateral flow as assessed at angiography. tively). A recent literature review found patients with CBS
Vessel occlusion is performed using coils or vascular typically have a history of radiotherapy (89%), nodal me-
plugs. Occlusions of the ICA can be performed just proxi- tastasis (69%), and neck dissection (63%).112 This disease
mal to the site of injury, although proximal and distal usually occurs proximal to the carotid bifurcation and
deployment is ideal, particularly when an arteriovenous is commonly associated with soft tissue necrosis in the
fistula is noted. For the vertebral artery, proximal and neck (55%) and mucocutaneous fistulas (40%). More than
distal occlusion should be undertaken to prevent the later 90% of patients with CBS are treated with endovascular
formation of an arteriovenous fistula (Fig. 20-19). If a therapy (Fig. 20-20); surgical ligation is rarely indicated.
fistula forms distal to the site of occlusion, subsequent Endovascular treatment consists of covered stent place-
embolotherapy may require difficult or treacherous nego- ment or occlusion of the carotid artery. The morbidity and
tiation through collaterals or the contralateral vertebral mortality rates of patients with CBS are significant.
artery coursing across the basilar and down the ipsilateral Although the internal carotid and vertebral arteries
vertebral artery. Following vessel occlusion, it is essential are commonly injured in penetrating trauma, the ECA is
to monitor the patient closely and administer appropriate the most common artery when one includes individual
medical therapy to control blood pressure, and maintain branch injuries113 (Fig. 20-21). Major vessel injury occurs
hydration and gradual increase in activity. even more often with blunt trauma. Branches of the ECA
Carotid blowout syndrome describes rupture of the ca- may be occluded but not require intervention. Trauma
rotid artery as a complication of aggressive surgery and may present as pseudoaneurysm, extravasation (includ-
radiation therapy for carcinoma of the neck. These treat- ing epistaxis), and/or arteriovenous fistula formation.
ments can result in poor wound healing, eventual expo- The standard endovascular therapy for trauma to the
sure of the carotid artery, and minor sentinel to frank ECA is proximal vessel occlusion, most often with coils.
628 V. MISCELLANEOUS VASCULAR INTERVENTIONS
A B
C D
FIGURE 20-19 Right vertebral artery to jugular vein fistula with vessel occlusion in an 18-year-old patient with a self-inflicted gunshot
wound to neck. A, Right anterior oblique angiogram of right vertebral artery shows arterial occlusion just above a relatively small fistula to the
jugular vein (arrows). The jugular vein is very lightly opacified (arrowheads). Given the patients condition and diminutive size of the arteriovenous
fistula with vertebral artery occlusion, endovascular therapy was not performed. B, Follow-up right vertebral artery angiography shows enlarged
arteriovenous fistula (arrow) to the jugular vein (arrowheads) with continued vertebral artery occlusion distal to the fistula. Left vertebral artery
angiogram demonstrated a normal left vertebral artery without retrograde flow down the right vertebral to the fistula site. C, Right vertebral
artery occlusion. Microcatheter was advanced above the fistula site in the right vertebral artery and coiling was performed above and below the
fistula (arrow). D, Left vertebral arteriography after coiling of right vertebral artery fistula site, confirming no-flow down the right vertebral
artery (arrows) to supply the arteriovenous fistula. Minimal contrast opacification of distal right vertebral artery (arrow) is normal with more
proximal occlusion.
20. NEUROINTERVENTIONS 629
A B
FIGURE 20-22 Spontaneous carotid artery dissection in a 44-year-old man with headache and left-sided Horner syndrome for 3 weeks.
A, Right common carotid angiogram shows dissection of right internal carotid artery extending to base of skull (arrows). B, Right common
carotid angiogram shows dissection of right internal carotid artery completely healed following 15 months of medical therapy consisting
of both warfarin and antiplatelet agents.
long-term symptoms are unusual (about 1%).118 More 5. Ong CK, Lam DV, Ong MT, et al. Neuroapplication of Amplatzer
invasive therapies are usually undertaken when medical vascular plug for therapeutic sacrifice of major craniocerebral arter-
ies: an initial clinical experience. Ann Acad Med Singapore 2009;38:763.
therapy fails. Primary surgical repair for spontaneous in-
6. Smith TP. Embolization in the external carotid artery. J Vas Interv
ternal carotid dissection is rarely performed because the Radiol 2006;17:1897.
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tion is often buried in the skull base. The better surgical ment of arteriovenous malformations: a multidisciplinary ap-
option is ICA bypass. The most attractive endovascular proach. J Vasc Surg 2004;39:590.
8. Vos JA, van den Berg JC, Ernst SM, et al. Carotid angioplasty and
option has been stenting the dissected segment with the
stent placement: comparison of transcranial Doppler US data and
goal to close the flap and restore true lumen patency. clinical outcome with and without filtering cerebral protection
Since this approach is only taken for patients who fail devices in 509 patients. Radiology 2005;234:493.
medical therapy, the numbers of reported cases is rela- 9. OHolleran LW, Kennelly MM, McClurken M, et al. Natural history
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67. Nogueira RG, Yoo AJ, Buonanno FS, et al. Endovascular approaches 2006;25:40.
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Stroke 2004;35:2848. broma. In: Barnes L, Eveson JW, Reichart P, et al, editors.
71. Bose A, Henkes H, Alfke K, et al. The Penumbra System: a mechani- World Health Organization Classification of Tumours: pathology &
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75. Wieneke JA, Smith A. Paraganglioma: carotid body tumor. Head 97. Mohammadi M, Saedi B, Basam A. Effect of embolisation on endo-
Neck Pathol 2009;3:303. scopic resection of angiofibroma. J Laryngol Otol 2010;124:631.
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100. Pope LER, Hobbs CGL. Epistaxis: an update on current manage- 111. Mathis JM, Barr JD, Horton JA. Therapeutic occlusion of major
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104. Kotecha B, Fowler S, Harkness R, et al. Management of epistaxis: embolization of vascular injuries of the face and neck. Laryngoscope
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110. Donas KP, Mayer D, Guber I, et al. Endovascular repair of extracra- SR121566A, a potent GP IIb-IIIa antagonist on platelet-mediated
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S E C T I O N VI
21
Gastrointestinal Interventions
Sandeep Vaidya, Gerant Rivera-Sanfeliz, Gregory Lim
637
638 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
FIGURE 21-1 Esophageal stent placement for malignant stricture. A, Esophagogram shows narrowing of the midesophagus secondary to
an excavating esophageal carcinoma. B, Widely patent esophagus following deployment of covered Wallstent.
640 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
patient is placed on antireflux measures that include The most common complication seen with covered
elevation of the head of the bed and pharmacologic stents is migration, whereas the most common complica-
acid suppression therapy. tion seen in uncovered stents is tumor in-growth (Fig. 21-2).
Ileus and perforation have been reported with stent mi-
RESULTS gration.45 To minimize migration, changes in stent design
Esophageal stent placement is technically successful in have been implemented that include covering inside the
97% to 100% of cases.33 Overall procedure-related morbid- metal mesh (exoskeleton), uncovered segments at both
ity and mortality with self-expanding metallic stents are ends (longer proximally), and larger proximal diameter
low.34-38 Dysphagia is relieved in 90% of patients who un- (cone-shaped stent). A device with some of these modifica-
dergo esophageal stent placement.39 Successful closure of tions is the Flamingo stent (Boston Scientific).
tracheoesophageal or bronchoesophageal fistulas can be
achieved in 70% to 100% of patients.40 Treatment failure
occurs more frequently when the esophagus is dilated, STOMACH
preventing stent-wall apposition, and when the fistula is
in proximity to the superior esophageal sphincter. Overall, Enteral Nutrition and Decompression
the reintervention rate is 25%.32
Background
COMPLICATIONS Malnutrition is a common problem affecting up to 40% of
Adverse events related to esophageal stent placement hospitalized patients, increasing their morbidity and
are uncommon. Major complications include bleeding mortality.46 Nutritional support can be given either enter-
(up to 6%), aspiration pneumonia, tracheal compres- ally or parenterally. Parenteral nutrition is costly and has
sions, perforations, and tracheoesophageal fistulas (up high risks of complications, including sepsis, hepatic dys-
to 8%). Minor complications include chest pain/discom- function, metabolic disturbances, catheter-associated vein
fort, tumor in-growth or overgrowth, stent migration thrombosis, and intestinal mucosal atrophy.47 Several stud-
(up to 35%), gastroesophageal reflux, hiccups, foreign ies have shown that enteral feeding has lower complication
body sensation, failure in stent expansion, granulation rates when compared with its parenteral counterpart.48,49
tissue formation, and food bolus obstruction (4% to Enteral feeding requires a functioning gut and can be
18%).41,42 Vocal cord paralysis and stent fracture have provided in the short term via nasogastric or nasojejunal
also been reported.43,44 The mortality rate associated tubes. In the long term, however, these tubes have high
with esophageal stent placement is approximately 0.5% complication rates, including mechanical problems, local
to 2%.39 erosions and aspiration pneumonia. Patients with chronic
A B C
FIGURE 21-2 Stent migration in the esophagus. A, Swallow study showing leak at the gastroesophageal junction (black arrow). B, First
follow-up computed tomography (CT) scan after an esophageal stent was placed to seal the leak shows good device position (black arrow).
C, Patient developed abdominal pain 6 months after stent placement. Reformatted coronal CT scan reveals that the stent has migrated
(black arrow).
21. GASTROINTESTINAL INTERVENTIONS 641
swallowing disorders or obstruction to swallowing, or intestinal obstruction. Less common indications include
those who are unable to ingest food because of head craniofacial abnormalities and impaired intestinal ab-
trauma or stroke, or those with anorexia resulting from sorption, requiring slow infusions of alimental diet into
underlying diseases such as cancer require more perma- the small bowel via a gastrojejunostomy or jejunos-
nent access by placement of a gastrostomy, gastrojejunos- tomy.52 Absolute contraindications to PG include uncor-
tomy, or jejunostomy. rectable coagulopathy and unsatisfactory anatomy (Box
Minimally invasive gastrostomy can be performed us- 21-3 and Fig. 21-3), such as an overlying colon or left lobe
ing endoscopic (percutaneous endoscopic gastrostomy of liver or the entire gastric lumen located above the cos-
[PEG]) or fluoroscopic (percutaneous gastrostomy [PG]) tal margin even after air insufflation.
guidance. The advantage of PG over PEG is that endos- The presence of a ventriculoperitoneal (VP) shunt was
copy is avoided, which is a significant advantage in considered a contraindication, but this notion has been
patients with an esophageal or pharyngeal obstruction. challenged. One study found a 9% VP shunt infection
In addition, sedation requirements are less during PG.
Wollman and colleagues published a comparison of surgi-
cal, endoscopic, and fluoroscopic techniques for gastrosto-
mies that included a metaanalysis of the literature.50 Their BOX 21-3
conclusion was that PG is associated with a higher success
rate than is PEG and with less morbidity than either PEG C O N T R A I N D I C AT I O N S
or surgery. More recently, Hoffer and colleagues performed T O P E R C U TA N E O U S
a prospective, randomized comparison and concluded that GASTROSTOMY
percutaneous gastrojejunostomy had a higher success rate
and fewer complications, whereas PEG took less time, cost Absolute Contraindications
less, and required less tube maintenance.51 Uncorrectable coagulopathy
Life expectancy less than 1 week
Percutaneous Gastrostomy (Online Video 21-1) Imminent abdominal surgery
Unsatisfactory anatomy
PATIENT SELECTION
The major indication for PG as a means of nutritional Relative Contraindications
support are listed in Box 21-2. PG also may be used for
gastrointestinal decompression. This indication is more Massive ascites
common in patients with carcinomatosis causing chronic Abdominal varices
Prior gastric surgery
Inflammatory, neoplastic, or infectious involve-
ment of the gastric wall
BOX 21-2 Severe gastroesophageal reflux
Ventriculoperitoneal shunt
I N D I C AT I O N S
F O R P E R C U TA N E O U S
GASTROSTOMY OR
GASTROJEJUNOSTOMY
Gastrostomy
Head and neck tumors or malignant esophageal
tumors
Swallowing impairment due to cerebrovascular
accident or neuromuscular disorder
Nutritional supplementation for chronic illness
or extensive surgery
Gastrojejunostomy
Severe gastroesophageal reflux and recurrent
aspiration
Functional or organic gastric outlet obstruction
FIGURE 21-3 Colon interposition between the stomach and
abdominal wall precludes placement of a percutaneous gastrostomy.
642 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
C D
A B
FIGURE 21-7 Placement of a needle (A) and T-fastener (B) for percutaneous gastrostomy under computed tomography guidance in a
patient with prior partial gastrectomy.
21. GASTROINTESTINAL INTERVENTIONS 645
B
FIGURE 21-8 Percutaneous gastrostomy for gastric outlet obstruction without T-fasteners. A, Axial (left) and coronal (right) computed
tomography (CT) images show gastric outlet obstruction. B, Axial CT images 12 hours after nonT-fastener gastrostomy show peritoneal
leakage and associated inflammation.
as an internal surgical staple. The operator may choose incidence of serious technical complications in the non-
to give intravenous antibiotics to cover skin flora in this gastropexy group that included four catheters that mi-
situation. grated into the peritoneal cavity.64 However, they also
Dewald and colleagues compared over 700 gastro- noted a 10% incidence of pain and 13% incidence of
pexy and nongastropexy gastrostomies and concluded skin excoriation at the T-fastener sites. Until recently, all
that no risk was added with gastropexy.63 Thornton and T-fasteners had nonabsorbable sutures, which necessi-
colleagues performed a randomized comparison of gas- tated follow-up for cutting these sutures so as not to
trostomies with and without T-fasteners and concluded form local stitch abscesses. With the advent of new
that fasteners should be used routinely based on a 10% designs that incorporate absorbable sutures, there may
646 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
be no need to ever cut the strings. However, there are few nical success of 95% for PEG and 100% for surgical
data to support the actual benefit of these new materials. gastrostomies.50 Technical failure results from lack of
The procedure is performed under fluoroscopic guid- safe access route, most commonly from overlying trans-
ance using an over-the-guidewire technique. Most inter- verse colon. Other reasons for inability to insert at PG
ventionalists prefer to place the tube with a retrograde include massive ascites, gastric cancer, peritoneal carci-
(push) technique, although antegrade (pull) tech- nomatosis, overlying open abdominal wound, and pre-
niques are favored by other practitioners. Indications for vious gastric surgery.
the pull method include insertion in patients who are at
high risk for pulling out the gastrostomy, who may desire COMPLICATIONS
a button device in the future, or who need a very large- A small pneumoperitoneum immediately after the proce-
bore tube.65 This technique requires retrograde catheter- dure is normal. Complications are uncommon. A recent
ization of the esophagus followed by exteriorizing the metaanalysis reported a 5.9% overall complication rate
wire through the mouth and delivering the catheter using and a 0.3% mortality rate for PG.50 By contrast, PEG was
an antegrade technique typical of PEG placement. How- associated with a 9.4% complication rate, whereas surgery
ever, the method poses a potentially increased risk for was associated with a complication rate of 19.9%.
stomal infections due to passage of the tube through the Peritonitis is a rare but serious complication following
oral cavity.66 gastrostomy and may follow leakage or inadvertent
Large-bore tubes can be inserted with standard push infusion of the nutrient into the peritoneal cavity. Early
radiologic technique by dilating the tract with a 10-mm detection, discontinuation of feedings, and antibiotics
diameter # 12-cm-long balloon, inserting a 24- to 26-Fr can control a minor leak. Contrast studies through the
peel-away sheath, followed by delivery of a 20- to 24-Fr tube may fail to show the defect, but an enlarging
MIC-type gastrostomy catheter.67 In one report, investi- pneumoperitoneum is considered to be a reliable sign
gators used a three-point T-fastener gastropexy in all of of intraperitoneal leakage.52
their 109 gastrostomies and concluded that percutane- Aspiration pneumonia secondary to gastroesophageal
ous large-bore catheter placement is safe and has the reflux has long been considered a major cause of morbid-
same technical success and morbidity and mortality ity and mortality in patients with feeding gastrostomies.
rates when compared with surgically or endoscopically Gastrostomies affect gastric emptying and, theoretically,
placed tubes, as well as small-bore tubes placed under may increase the risk for aspiration.69 However, Olson
fluoroscopic guidance. and colleagues found no causal relationship between gas-
trostomy tube placement and gastroesophageal reflux.70
POSTPROCEDURE CARE They recommend PGJ placement only in patients with
Patients remain fasting for the following 24 hours. preexisting moderate to severe reflux or who are at high
They are observed for 4 hours for abdominal pain, risk for aspiration pneumonia.
distention, and bleeding. The catheter is placed to Bleeding following PG placement usually is self-limited
gravity drainage or to low intermittent suction for but can be significant in patients with an underlying
24 hours to decompress the stomach and monitor for coagulopathy. If bleeding persists, direct arterial injury
bleeding complications. Twenty-four hours later, tube should be suspected. Other etiologies include gastritis or
feeding can start gradually if there are no signs of peri- gastric ulceration.
tonitis (fever, abdominal pain, tenderness) and there In some instances, the tube may get pulled in along
are good bowel sounds. Tolerance and progression can with the flange/bumper due to peristalsis, resulting in the
be assessed using residual volume measurements ev- flange/bumper digging into the skin and subcutaneous
ery 6 hours, with full nutrition generally achieved within tissue. The so-called buried bumper can result in second-
48 hours. However, results from various randomized ary infection of the skin and subcutaneous tissue. In this
clinical trials indicate earlier feeding (!3 hours) may be case, the infection can be deeper and hence more serious
safe for endoscopically placed devices.68 T-fasteners than a simple skin site infection. Buried bumper syndrome
are cut in 7 to 10 days. Catheter care instructions are is a potentially serious complication of percutaneous gas-
given to the patient and caregivers, including informa- trostomy tube placement.71
tion about tube feedings, catheter maintenance, and Wound infections after PG are not uncommon and occur
how to recognize signs and symptoms that may herald within days to months following tube placement. They are
complications. treated with local care and antibiotics. In this respect, PG
differs from PEG, in which the latter has a higher frequency
RESULTS of skin infections because the tube is contaminated by oral
Technical success rate for PG is 95% to 100% and the flora as it is passed through the mouth and oropharynx on
procedure-related mortality rate varies between 0% and its way to the stomach.72-74 Overall PG and PEG seem to
3.2%.52 A metaanalysis of the literature reported a tech- have similar 30-day and 1-year mortality rates.
21. GASTROINTESTINAL INTERVENTIONS 647
Tube malfunction or dislodgment is treated with tube given in boluses and prepared at home with a blender;
replacement, which should be accomplished within a patient tolerance is excellent. Jejunal feedings, on the
day or so before the track has closed. To prevent fre- other hand, require nutrient solutions prepared in a
quent occlusion, vigorous tube flushing must be per- pharmacy and delivered by a pump; patient tolerance is
formed after each use, particularly when dealing with variable. Tolerance to enteral nutrition may be improved
small-bore gastrostomies. by tailoring the solutions volume, rate, and concentra-
tion to the individuals condition.
Percutaneous Transgastric Jejunostomy
and Gastrojejunostomy TECHNIQUE
Some interventionalists prefer jejunal placement of The gastric puncture should be directed toward the py-
feeding tubes, citing the high prevalence of pulmonary lorus. Direct puncture into the antrum should be avoided
aspiration in chronically ill patients and the fact that to prevent potential impairment of gastric emptying
gastrostomies adversely affect gastric emptying, which function. Placement of the transgastric jejunostomy
may increase the risk of aspiration even further.69 Pri- is relatively straightforward unless there is gastric outlet
mary placement is often done using the pigtail retention obstruction. In that case, some degree of manipulation
tube (e.g., 14-Fr Shetty catheter, Cook Inc.). The pigtail may be needed with shaped catheters and a wire to cross
catheter is sometimes exchanged for a balloon-retention the pylorus and achieve a suitable position.
catheter at a later date (Fig. 21-9). Placing a fresh large-bore dual-lumen gastrojejunos-
tomy tube can be fraught with problems. More com-
PATIENT SELECTION monly, a gastrostomy tube is placed and then converted
PGJ is preferred in some circumstances. If direct jejunal to a dual-lumen balloon retention gastrojejunostomy tube
feeding is required due to gastric pathology, a transgastric after 2 to 4 weeks when the track is mature62 (Figs. 21-10
jejunostomy (with jejunal endhole only) will suffice. and 21-11). If a transgastric jejunostomy tube is indicated,
When gastric decompression needs to occur in addition to the interventionalist is limited to the Marx-Cope device
jejunal feeding, the tube configuration is a coaxial one (Cook Inc.), which is a 16-Fr pigtail catheter with a side
with the gastric portion or hub having the decompressive port for a 5-Fr jejunal tube. The gastric portion is inserted
holes in the stomach while the jejunal feeding portion re- in the regular manner. The jejunal portion is then manipu-
sides beyond the ligament of Treitz. lated through this tube, exiting the side port and then
There are marked differences between gastrostomy crossing the pylorus (see Figs. 21-10 and 21-11). The jeju-
and gastrojejunostomy feedings. Gastric feedings can be nal limb is prone to occlusion due to its small caliber.
A B
FIGURE 21-9 Transgastric balloon retention jejunostomy tubes. A, Primary placed 14-Fr Shetty gastrojejunostomy tube. Arrow indicates
retention loop, which is ideally positioned beyond the pylorus. The distal catheter should lie beyond the ligament of Treitz. B, Later replace-
ment with a balloon-retained (arrow) transgastric jejunostomy tube.
648 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
FIGURE 21-10 Balloon-retained dual-lumen gastrojejunostomy tube. This device is usually inserted after primary gastrostomy tube
placement. Arrow indicates the retention balloon. Gastric port injection (A) and jejunal portion injection (B).
A B
antileak mechanism. Some surgeons may additionally abdominal wall is selected for access. Occasionally, it
invaginate about 2 cm of the tube on the bowel wall may be necessary to decompress overlying large bowel
and anchor it to the serosa with sutures. However, this loops. Access is gained using a 21-gauge needle, and
makes it much more difficult to replace percutane- stay fasteners are delivered. Intraluminal positioning
ously, if necessary, using the Seldinger technique. The can be confirmed by gentle contrast injection. The tract
outer end of the tube is exteriorized through the is then dilated and a 10- or 12-Fr pigtail catheter is
abdominal wall at a site distant from the laparotomy placed.84,87,90
incision. However, surgical jejunostomy can be associ- Care should be taken not to create torsion during de-
ated with significant morbidity and mortality.78 In ad- ployment of the locking tube, and emphasis should be
dition, patients usually are poor surgical candidates placed on correctly sizing the diameter of the catheter
because of chronic illness, debilitated state, or poor loop with the target segment of jejunum. Feeding can be
nutritional status. started 24 hours following the intervention.
Direct percutaneous endoscopic jejunostomy can be per- A dislodged surgical jejunostomy can be replaced
formed in patients who have had gastric surgery with a percutaneously. Success is more likely if attempted less
gastroscope; otherwise, a long enteroscope is needed than 10 days after dislodgment or removal of the tube
to reach the first 2 feet of jejunum.79 In addition to access and when the original tube was in place for more than
issues, it may be difficult to transilluminate the abdomi- 4 weeks for the tract to mature. Hietmiller and col-
nal wall through a deeply seated or easily mobile bowel. leagues recommend marking the jejunopexy site at sur-
The failure rate can be as high as 14%, and the procedure gery with radiopaque markers to assist visualization
can be complicated by colonic perforation or abdominal if re-access is needed.93
wall abscess.79
Laparoscopic jejunostomy requires general anesthesia, RESULTS AND COMPLICATIONS
absence of significant intraabdominal adhesions, and a With experience, the technical success rate of percutane-
skilled operator. In two series, there was a conversion ous jejunostomy approaches 95%. Minor complications
rate to open surgery of 8% to 12.5% and a serious com- included localized pain, infection at the insertion site,
plication rate (including volvulus) of 11% to 25%.80,81 and tube occlusion.87,90 Major complications include peri-
catheter leakage and peritonitis or abdominal abscess
TECHNIQUE formation. Data reported by van Overhagen and col-
Percutaneous jejunostomy (PJ) can be performed de novo leagues91 as well as Yang and associates88 showed that
or through a previous jejunostomy site. Gray and col- peritonitis occurred in about 13% of cases, all of which
leagues were first to describe this approach. Several tech- were managed nonoperatively. A 30-day mortality of
nical reports have since confirmed its feasibility and safety 5% to 17% has been reported.87,88,91
for feeding, decompression, and the management of bilio- The jejunostomy tube can be subsequently upsized if
enteric anastomotic strictures.82,83 PJ is more challenging needed. With proper management, these catheters will
than PG because of mobility and easy compressibility of function for long periods of time. Richard and cowork-
the jejunum. Technical success rates vary between 85% ers calculated a primary patency of 95% from a large
and 95%, with most of the failures resulting from difficulty series with mean follow-up of 285 days.86
in puncturing the bowel loop and loss of access during
dilatation for tube placement.84-88 Nasojejunal Tube Placement
Fluoroscopy in frontal and lateral projections is rou- Nasojejunal (NJ) tubes are used for temporary nutri-
tinely used for guidance. CT fluoroscopy (or even ultra- tional support in patients at risk of aspiration pneumo-
sound) guidance recently has been suggested to facilitate nia, patients intolerant of gastric feeding, patients with
the visualization and catheterization of mobile, anteriorly recurrent emesis or severe reflux, and patients who have
positioned, unopacified, or nondistended bowel.84,87,89-91 undergone major surgery or sustained severe trauma.94
Most interventionalists agree that appropriate bowel NJ tubes can be placed at the bedside, with fluoroscopic
distention and the use of T-fasteners are two important guidance, or via endoscopy.95
factors for the technical success of percutaneous jejunos- Care is taken to anesthetize the nasopharynx and oro-
tomy.92 Bowel distention can be achieved with a naso- pharynx with Cetacaine (benzocaine; tetracaine) spray
gastric or nasoduodenal tube. A 5-Fr catheter is usually and Xylocaine (lidocaine) jelly, which is injected into the
placed into the proximal jejunum, either from the nose or selected nostril. Using fluoroscopic guidance, a long di-
through an existing PG, and is used for jejunal inflation agnostic catheter (4- or 5-Fr Kumpe or vertebral) and
using either saline or, more commonly, air. A catheter guidewire are manipulated through the pylorus past the
with an occlusion balloon may be used to increase the ligament of Treitz. An exchange-length guidewire is
intraluminal pressure and provide a target for the needle advanced and an NJ tube (Cook, Inc.) is delivered over
puncture. A suitable bowel loop that is close to the the guidewire.
21. GASTROINTESTINAL INTERVENTIONS 651
COLON
A B
C D E
FIGURE 21-13 Colonic stent placement for temporary decompression in preparation for single stage surgery. A, Plain abdominal radiograph
shows large bowel dilation secondary to obstructing distal descending colon carcinoma. B, Guidewires and catheters are manipulated across
the obstruction. C, Deployment of Wallstent is initiated. D, Deployment is completed. E, Abdominal film 12 hours after the procedure shows
successful relief of obstruction. The stent was not dilated with a balloon.
21. GASTROINTESTINAL INTERVENTIONS 653
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C H A P T E R
22
Biliary System
Steven C. Rose
Percutaneous invasive procedures involving the biliary segmental nomenclature has been described by Gazelle
system are designed to prove, characterize, and treat sus- and colleagues.5
pected biliary obstruction and, occasionally, biliary leaks.
Huard provided the initial description of transhepatic
cholangiography (THC) in 1937.1 Remolar and coworkers TRANSHEPATIC CHOLANGIOGRAPHY
first described external percutaneous biliary drainage
(PBD) in 1956.2 Nevertheless, these procedures did not
become widely accepted until the late 1970s, when skinny-
Patient Selection and Preparation
needle puncture techniques and coaxial exchange systems Given the widespread use of advanced cross-sectional
were developed to minimize the incidence of serious imaging and ERCP, nearly all patients have THC in
procedure-related hemorrhagic complications. Since their conjunction with PBD. The primary indication for THC is
development in the late 1980s, endoscopic retrograde to confirm, localize, and characterize obstructive disease
cholangiopancreatography (ERCP) and subsequently of the biliary system in patients with symptoms of pruri-
transendoscopic biliary drainage have diminished the tus or cholangitis who are not amenable to ERCP. 6
need for THC and PBD. Percutaneous therapy continues Increasingly, magnetic resonance (MR) cholangiography
to have a role in patients with anatomy unfavorable to is being used to image the biliary system noninvasively.7,8
endoscopic procedures and in institutions without skilled Occasionally, THC and PBD are used as part of the non-
interventional endoscopists.3 operative management of patients with biliary leaks from
bile duct injuries.
In addition to establishing the presence of biliary
NORMAL ANATOMY obstruction, cholangiography can localize the obstruc-
tion and frequently suggests the benign or malignant
The bile ducts of the posterior and anterior segments cause of the stricture. However, the cholangiographic
of the right hepatic lobe join near the porta hepatis to form appearance may be misleading. The final diagnosis rests
the main right hepatic duct. The bile ducts of the medial on tissue analysis. In patients who are candidates for
and lateral segments of the left hepatic lobe merge to operative resection and biliary-enteric decompression,
become the left main hepatic duct.4 The right posterior the tissue diagnosis usually is made from the operative
and right anterior segmental bile ducts join the left main specimen. In cases managed nonoperatively, the tran-
hepatic duct directly in about 25% and 6% of individuals, shepatic access is a convenient route for obtaining the
respectively. The right and left main hepatic ducts coalesce necessary material.
in the hilum to form the common hepatic duct. At the The relative benefits and risks of THC are weighed
porta hepatis, the bile ducts run anterior to the hepatic against those of endoscopic and operative diagnostic
artery and portal vein. The gallbladder empties into the methods. Primary factors in the selection of patients
cystic duct, which is joined by the common hepatic duct to include the suspected anatomic level, cause of biliary
become the common bile duct (CBD), which travels within obstruction, and the availability of highly skilled
the hepatoduodenal ligament to drain through the sphinc- practitioners.
ter of Oddi into the duodenum. A number of potential Most distal (periampullary) bile duct obstructions
aberrant communications exists between the biliary tree are managed endoscopically. Middle (extrahepatic
and the gallbladder. The complex relationship between and extrapancreatic) CBD lesions typically undergo
the biliary ductal system and the Couinaud hepatic operative resection with creation of a biliary-enteric
656
22. BILIARY SYSTEM 657
A B
FIGURE 22-2 Biliary branching pattern. Shaded surface display of a spiral computed tomography cholangiogram performed through an
indwelling left-sided percutaneous biliary drainage catheter in a patient with pancreatic adenocarcinoma. A, Right anterior oblique view displays
the pinnate-type (feather-like), left-sided branching pattern. B, Inferior view depicts palmate-type (maple leaflike), right-sided branching pattern.
more cephalad entry point frequently is required by the at approximately the right midclavicular line to avoid
position of the inferior margin of the right lobe of the inadvertent puncture of left-side bile ducts, through
liver or the anticipated location of the porta hepatis. which it would be nearly impossible to negotiate a
Fluoroscopy is used to assess the costophrenic sulcus guidewire or catheter toward the CBD.
during full inspiration to guarantee that the lung does The needle stylet is removed, and a small-volume
not cross the projected access route. The needle is passed syringe (e.g., 1 to 5 mL) with 60% strength contrast me-
over the superior aspect of a given rib to minimize the dium is attached. Small aliquots (e.g., 0.1 to 0.2 mL) of con-
risk for injury to the intercostal arteries. Under fluoro- trast material are delivered while the needle tip is slowly
scopic guidance, the needle is then directed along a retracted under fluoroscopy. If the contrast material re-
plane parallel to the tabletop and aimed toward the mains as a smudge at the needle tip, the tip is located in
11th thoracic vertebral body. If the same access may be the liver parenchyma, and it should continue to be with-
used for biliary drainage, the needle pass should stop drawn. If contrast medium enters a tubular structure but
Ultrasound
transducer
A B
FIGURE 22-3 Sonographic guidance for left-sided transhepatic cholangiography and percutaneous biliary drainage. A, The ultrasound
probe has a transverse orientation along the axis of the left-sided bile duct and adjacent hepatic artery and portal vein. The skinny needle
courses along the sonographic imaging plane to selectively enter the bile duct. B, The transverse sonogram depicts the needle course (arrows)
through the liver and into the dilated left-sided bile duct.
22. BILIARY SYSTEM 659
then flows readily away, the needle tip probably resides instillation of 5 to 10 mL of contrast material permits
within a vascular structure and withdrawal is continued. diagnostic cholangiographic images while minimizing
If contrast material fills a tubular structure and remains in the risk of bacteremia and possible gram-negative sepsis.
the region of the needle tip, the tip probably is within If a biliary leak is suspected, full-strength (60%) contrast
the biliary system. Injection of an additional 5 to 10 mL material is warranted to visualize the fistula. However,
should confirm the intrabiliary location and determine the if intraluminal filling defects (e.g., stones) or disease with
ductal diameter and relationship to the porta hepatis and subtle bile duct wall abnormalities (e.g., sclerosing chol-
obstructive lesions. angitis) is suspected, 60% contrast medium should be
Left-sided access originates from the left subcostal diluted by one half with normal saline solution. The
aspect of the epigastrium. Sonographic guidance permits biliary system should be aspirated before removal of the
direct visualization of the skinny needle as it is directed skinny needle if drainage is not planned.
into an acceptable left bile duct while minimizing the
likelihood of traversing the adjacent left hepatic artery or
Imaging Findings
left portal vein branch (Fig. 22-3). Aspirated bile should
be sent for routine Gram stain, culture, and sensitivity Most pathologic processes of the biliary tree are mani-
tests; if infectious complications arise, informed choices fested in a few forms17-23
can be made regarding antimicrobial therapy.
If a diagnostic THC is to be performed without subse- Abnormally small-caliber bile ducts or occlusion of
quent PBD, removal of 5 to 10 mL of bile alternating with the bile ducts (Table 22-1; Figs 22-4 through 22-11)
Text continued on p. 664
Pseudostricture due to positional underfilling of contrast Supine: narrow proximal (hilar) CBD and nonopacified left bile
material (see Fig. 22-4) ducts
Prone: narrow distal CBD and nonopacified right bile ducts
Eliminated by positional changes
Pseudocalculus due to mucosal prolapse (see Fig. 22-5) Distal CBD meniscus
Mimics stone or polyp
Intermittently disappears as sphincter opens
Cholangiocarcinoma (see Fig. 22-6) Usually located near or associated with hilum
Usually occlusive
Usually abrupt margin
Nodular surface
Pancreatic or ampullary carcinoma (see Fig. 22-7) Located at distal CBD
Fixed lesion
Rat tail appearance
Usually occulsive
Extrinsic adenopathy Usually hilar or suprapancreatic CBD
Nonspecific
May have smooth surface
Fibrosis (see Fig. 22-8) Located at biliary-enteric or biliary-biliary anastomosis, site of
injury, papilla, or in proximity to stones
Usually short segment
Usually smooth
Sclerosing cholangitis (see Fig. 22-9) Multifocal strictures
Intrahepatic and extrahepatic
May have diffuse narrowing
Often mural diverticular outpouching
Ischemic or AIDS-related cholangitis (see Fig. 22-10) Ischemic or chemotoxic structures
Similar to sclerosing cholangitis, papillary stenosis, or both
Patients with liver transplant or
liver malignancy and transcatheter chemoinfusion or
chemoembolization
Multifocal, diffuse intrahepatic strictures
May have anastomotic stricture
May have associated sloughed debris, leaks
Recurrent pyogenic cholangitis (Oriental cholangitis) Multiple intrahepaic strictures
(see Fig. 22-11) Upstream dilation, especially left lobe
Usually associated with innumerable stones
A B
FIGURE 22-4 Artifactual nonopacification of bile ducts caused by underfilling with contrast material, which has a higher specific gravity
than bile. A, T-tube cholangiogram in a supine patient. The nondependent common hepatic duct (arrow) appears narrow, and the left-sided bile
ducts did not fill at all. B, Endoscopic retrograde cholangiopancreatography in a nearly prone patient. The nondependent distal common bile
duct appears narrow (between curved arrows). Right-sided ducts (straight white arrow) are not opacified. The irregular filling defect (small black
arrows) in the distal common bile duct is viscous bile.
A B
FIGURE 22-5 Mucosal prolapse. A, A polypoid filling defect is identified in the distal common bile duct (arrow). B, A few minutes later, the
sphincter has opened (arrow).
22. BILIARY SYSTEM 661
FIGURE 22-6 Cholangiographically guided transluminal FIGURE 22-7 Malignant stricture in the common bile duct
biopsy of hilar cholangiocarcinoma using a myocardial biopsy caused by pancreatic carcinoma. The stricture has a rat-tail or
forceps (straight arrow) introduced through a vascular-type beaked appearance (curved arrow), typical of malignant periampullary
percutaneous transhepatic sheath (curved arrows). strictures.
A B
FIGURE 22-8 Expandable metallic stent for a benign tuberculous stricture. Contrast-enhanced computed tomography scan showed
dilation of intrahepatic bile ducts bilaterally. The extrahepatic bile ducts were normal. A, Left anterior oblique view of a cholangiogram
performed through a bilateral percutaneous biliary drainage catheter defined a near-occlusive eccentric stricture (arrows) of the hilar portion of
the common bile duct, which had been retracted posteriorly, presumably because of fibrosis. B, After attempted percutaneous cholangioplasty,
which failed because of elastic recoil, an 8-mm-diameter, 40-mmlong Wallstent (arrows) was deployed successfully. The left anterior oblique
view documented excellent stent position and expansion.
FIGURE 22-9 Sclerosing cholangitis. Cholangiogram through an indwelling
T-tube shows multiple strictures of intrahepatic and extrahepatic bile ducts.
Scattered normal segments of intrahepatic bile ducts are seen upstream from the
strictures; otherwise, intrahepatic ducts are of small caliber. Subtle diverticula
(arrows) of the strictured common hepatic duct are detected, and the surgical clips
are from a cholecystectomy.
A B C
A B
C D
FIGURE 22-11 Staged multimodality management of complex biliary disease (recurrent pyogenic cholangitis). A, Endoscopic retrograde cholangio-
pancreatography (ERCP) demonstrated multiple hilar biliary strictures (arrows), dilation of multiple intrahepatic bile ducts, and innumerable biliary calculi
located within a massively dilated left bile duct. Pneumobilia resulted from prior endoscopic papillotomy. B, Magnified view of the abdominal computed
tomography scan after the ERCP confirmed the hilar biliary strictures (arrows), bile duct dilation, and calculi. C, After bilateral biliary drainage, balloon
cholangioplasty of the hilar biliary strictures, multiple sessions of basket retrieval of pigmented biliary calculi, and oral administration of ursodeoxycholic
acid, the cholangiogram demonstrated improvement in the hilar biliary luminal diameter, partial resolution of the intrahepatic bile duct dilation, and
near-complete removal of the calculi. D, After successful transluminal therapy, the bilateral percutaneous biliary drainage catheters have been converted
to a long-term indwelling Silastic U-tube (arrows) to preserve transhepatic biliary access. (Courtesy of Thomas Kinney, MD, and Horacio DAgostino, MD,
University of California, San Diego, Medical Center.)
664 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
Obstruction (see Figs. 22-7 and 22-8) Diffuse, though may disproportionately affect extrahepatic or left lobe ducts
Upstream from obstructing structure (stricture, stone)
Prior obstruction History of treated obstruction
Contrast material flows to bowel
May need manometry to distinguish from true obstruction
Choledochal cysts
Type I (80%-90%) (see Fig. 22-12) Extrahepatic CBD
Fusiform, single
Type II (2%) (see Fig. 22-13) Extrahepatic CBD
Saccular or diverticular, single
Type III (1%-5%) Intraduodenal, single
Choledochocele
Type IV Multiple cysts
Usually intrahepatic and extrahepatic
Type V (see Fig. 22-14) Caroli disease
Single or multiple
Intrahepatic or extrahepatic bile ducts
Associated with hepatic fibrosis, renal cysts, renal tubular ectasia
Late phase ischemic injury (see Fig. 22-10) History of liver transplantation
Central biliary ectasia with debris*
Peripheral pruning of intrahepatic bile ducts
Denervation History of liver transplantation
Diffuse dilation
May have sphincter of Oddi dysfunction
Oriental cholangiohepatitis (see Fig. 22-11) Listed in Table 22-1
From Silverman SG, Coughin BF, Selzer SE, et al. Current use of screening laboratory tests before abdominal interventions: a survey of 603 radiologists. Radiology 1991;181:669.
CBD, common bile duct.
A B
FIGURE 22-15 Air bubbles at cholangiography. A, An air bubble is seen within the T-tube (small arrow). The bubble shape conforms to the
wall of the common bile duct and to other bubbles (between curved arrows). B, Continued injection of contrast material expels the bubbles from
the distal duct. The three bubbles in the common hepatic duct have coalesced into a single large bubble (arrow).
TABLE 22-4 Biliary Duct Leakage tip is then cut off and placed in a fixative solution.
Another technique for obtaining cytologic material is
Disease or Cause Suggestive Findings
fluoroscopically guided percutaneous skinny-needle
Elevated intraluminal pressure Downstream stricture aspiration (Fig. 22-20). Using the THC or PBD access,
(obstruction) (see Fig. 22-18) Hepatic abscesses or cholangiography is performed to localize the stricture.
suppurative cholangitis
Through a second percutaneous approach (usually ante-
Poor ductal wall integrity History of right upper quadrant
Bile duct injury surgery or injury, hepatic rior subcostal), a skinny needle is advanced using fluoro-
Dehisced biliary artery thrombosis, or scopic guidance to sample the identified stricture.
anastomosis or cystic duct irradiation Higher diagnostic yields for proving benign or ma-
stump lignant disease come from histologic examination of
Ischemia Associated with bilomas,
larger tissue samples because cellular architecture can
intrahepatic or extrahepatic
abscesses, ascites, and fistulas be evaluated. To accommodate the larger transluminal
to bowel, skin, or wounds biopsy devices, a vascular access sheath is placed into
Radiation therapy May be associated with the biliary system through the transhepatic route. The
downstream strictures hemostatic valve permits passage of the device while
contrast material is injected through the side arm port
to guide the biopsy.
Aspirated bile may be collected for cytologic examina- Currently available devices suitable for endoluminal
tion. Cytologic material also can be obtained using a biliary biopsy are flexible forceps developed for trans-
miniature brush biopsy device mounted on a guidewire26 venous biopsy of the myocardium27 (see Fig. 22-6). The
(Fig. 22-19). The brush biopsy device is introduced flexible transjugular liver biopsy needle (Cook Inc.,
through an angiographic catheter with the brush passed Bloomington, Ind.) should not be used because it is
intraluminally to and fro across the stricture. The brush designed to penetrate several centimeters beyond the
A B
C
FIGURE 22-18 Biliary leak. A, Cholangiogram performed through the left internal-external drainage catheter shows extravasation of
contrast (straight arrows) along a prior right-sided biliary drainage track and an obstructive stricture at the choledochojejunostomy anastomosis
(curved arrows). B, A large subcapsular hepatic abscess (arrows) is identified by contrast-enhanced computed tomography (CT). Percutaneous
drainage of the abscess was performed with initial return of thick, purulent material, which later converted to bile. C, Another CT scan 12 days
later documents successful treatment of the abscess (arrows) by simultaneous diversion of bile through the left percutaneous biliary drainage
catheter and drainage of the infected biloma. The biliary-enteric anastomotic stricture was treated with balloon cholangioplasty.
668 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
C D
670 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
After the biliary drainage catheter is positioned, it must drain externally through the catheter lumen into a
is secured in two locations: intraabdominally, using the drain bag. External drainage using siphonage is the most
locking pigtail tip of the catheter looped within the dilated effective transcatheter method for decompression of the
bile duct or bowel, and at the skin, using sutures or vari- biliary system and, therefore, is usually indicated in pa-
ous adhesive devices to secure the catheter to the abdomi- tients with evidence of suppurative cholangitis or severe
nal wall. The catheter is then attached to a drainage bag liver dysfunction from long-standing biliary obstruction.
for at least overnight external-type decompression. The An external PBD is flushed and exchanged easily. How-
catheter and tubing of the drainage bag need to be fluid ever, it is the least secure of the three drainage options, is
filled and the drainage bag placed in a more dependent a nuisance for the patient and caregivers because of the
position than the patients bile ducts to allow siphonage drain exiting the body and the required drainage bag, and
to occur effectively. The drain should be flushed with is associated with the loss of biliary fluids, electrolytes,
approximately 10 mL of sterile saline solution two to and bile salts. Serum fluid and electrolyte status need to be
three times daily and the biliary output recorded. monitored and replaced as needed. In the malnourished
patient, bile may be collected and administered orally to
Selection of Biliary Drainage Route assist with fat and fat-soluble vitamin absorption.
Fundamentally, three types of biliary drainage exist: ex- Internal-external PBD involves a percutaneous trans-
ternal, internal-external (universal), and internal. Each hepatic catheter that traverses the obstructive lesion
option has advantages and disadvantages. The choice of and has side holes proximal and distal to the site of
drainage mechanism should reflect the patients clinical obstruction (Fig. 22-23). Frequently, a locking pigtail tip
situation and lifestyle, the anatomy and pathology of the secures the downstream (central) portion within the
underlying stricture or leak, the patients life expectancy, bowel. When attached to a drainage bag, bile is han-
and planned adjunctive or operative therapy. dled by entering the upstream side holes and exiting by
In external PBD, all catheter side holes are located up- the transhepatic catheter shaft into a drainage bag. Al-
stream from the site of obstruction, usually along the in- ternatively, when the PBD catheter is capped, bile that
side curvature of the pigtail loop (Fig. 22-22). The catheter enters the upstream side holes is diverted across the
shaft passes out the abdominal wall. Bile, by necessity, site of obstruction to be dumped into the downstream
A B
FIGURE 22-22 External-type biliary drainage. A, The catheter position relative to the site of obstruction and the mandatory external
direction of bile flow into the attached bile bag are illustrated. B, Right and left external biliary drains in a patient with suppurative cholangitis
caused by an obstructing hilar carcinoma (i.e., Klatskin tumor).
22. BILIARY SYSTEM 671
C
A
CBD or small bowel. Advantages of internal-external stricture and allows bile to flow directly into the bowel
PBD include improved catheter security relative to (Fig. 22-24). No drain exits the body wall. Advantages
external drainage, avoidance of a drainage bag, easy include a high degree of security (i.e., no catheter shaft
catheter exchange over a guidewire, and excellent ac- to entangle passing objects or be grasped by delirious
cess for adjunctive treatment of benign or malignant patients); physiologic use of biliary fluid, electrolytes, and
strictures. Disadvantages include frequent occlusion bile salts; and optimized lifestyle (i.e., no exiting catheter,
of the catheter by debris (usually mucus produced by required flushing, or drainage bags). Significant disad-
the small bowel) and the catheter shaft exiting the vantages include the loss of access for adjunctive biliary
body, which may be distasteful or limit some patients intervention (i.e., any transcatheter adjuncts should
lifestyles. be considered before conversion of internal-external
Internal PBD involves a conduit (i.e., plastic tube or drainage to complete internal-type drainage) and loss of
expandable metallic stent) that traverses the obstructive ability to exchange occluded drainage systems altogether
672 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B C
FIGURE 22-24 Internal-type biliary drainage. A, Bile flows from the common bile duct (CBD) through the plastic internal biliary endo-
prosthesis into the duodenum. B, Radiograph of an endoscopically placed 10-Fr plastic endoprosthesis (arrows) after the endoscope has been
removed in a patient with CBD obstruction by pancreatic head adenocarcinoma. C, Expandable metallic stent for internal biliary drainage.
(i.e., expandable metallic stents) or dependency on trans- patients with benign strictures, probably because of
endoscopic exchange (i.e., plastic endoprostheses). poorer overall health, longer duration of intubation,
and the likelihood of bacterial colonization in patients
with malignant biliary obstruction.47
Results and Complications Minor procedure-related complications occur in 20%
Reported technical success for external and internal- to 30% of procedures. Delayed complications are prob-
external PBD ranges from 94% to 97% in patients with ably a function of the type of PBD drainage, catheter
dilated bile ducts and approximately 70% in patients with hygiene, and duration of intubation. Complications in-
nondilated bile ducts.6,40-42 Complications may be minor clude catheter occlusion, catheter dislodgment, and
or life threatening. Major periprocedure complications suppurative cholangitis.
primarily are caused by hemorrhage (usually hemobilia)
and infection (i.e., sepsis, suppurative cholangitis, or he-
patic abscesses) and occur in 4% to 8% of cases.6,40-45 Mas- TREATMENT OF BENIGN BILIARY
sive hemobilia may be caused by fistulous connections STRICTURES
between the hepatic artery or portal vein branches and
the biliary tree. Hepatic arterial injury is diagnosed with
Patient Selection
hepatic arteriography and treated with transcatheter
embolization.45 During arteriography, the biliary drain Appropriate case selection for treatment of benign
may need to be removed over a guidewire to identify the strictures centers on the likelihood of restenosis and the
point of contrast extravasation. If no hepatic arterial inju- results of alternative methods. Most patients with peri-
ries are identified, a portal vein injury is probable and is ampullary benign strictures should undergo endoscopic
treated with placement of a second transhepatic biliary sphincterotomy. Surgical biliary-enteric diversion pro-
drain, followed by embolization of the initial transhepatic vides better long-term patency than does cholangioplasty
tract, usually with a combination of angiographic coils or placement of expandable metallic stents in patients
and large Gelfoam torpedoes, cyanoacrylate glue, and with anastomotic or extrahepatic, extrapancreatic biliary
Onyx liquid embolic material46 (Fig. 22-25). An alternative strictures, particularly if the stricture has not been re-
technique involves obtaining ultrasound-guided access paired previously and the surgeon is highly experienced.
into the intrahepatic portal venous system, then selective Because of the lack of viable surgical alternatives short
embolization of the injured portal vein branch. of liver transplantation for treatment of intrahepatic
Procedure-related fatality is reported in 1% to 6% biliary strictures, percutaneous treatment is warranted in
of patients who undergo PBD.40-42 In patients with ma- patients with dominant strictures caused by sclerosing
lignant strictures, however, fatal and major nonfatal cholangitis, nonanastomotic strictures after liver trans-
complications are two to three times higher than in plantation, and other benign intrahepatic strictures.48-53
22. BILIARY SYSTEM 673
A B
C D
FIGURE 22-25 A, Track embolization to treat biliary-portal venous fistula. Abdominal computed tomography with original internal-external
biliary drain (arrow) traversing branch of right portal vein. B, Cholangiogram through vascular sheath in transhepatic track opacifying both the
biliary system (B) and the right portal vein (PV). C, After placement of a second internal-external biliary drain (2) prior to sacrificing original
biliary drain (1). D, Cholangiogram through the second biliary drain. A metallic coil (arrowhead) placed into the track dislodged into the biliary
system (subsequently passed into bowel). The track was then sealed with Onyx 34 (arrows) delivered through an angiographic catheter.
Recently introduced covered stents may hold prom- Primary patency rates range from 73% to 92% at 6 months,
ise for improved long-term patency compared with 66% to 75% at 12 months, 40% to 59% at 24 months, 22%
bare metallic stents or repeated balloon cholangioplasty. to 38% at 48 months, and up to 9% at 60 months. Depend-
One surface of the stent is covered with a thin layer of ing on the duration of follow-up, 13% to 60% of patients
fabric with very small pore size (approximately 1 !m) require reintervention, with resulting secondary patency
to minimize biliary epithelial ingrowth and adherence rates of 69% to 88% at 3 to 5 years.54 Because most patients
of debris.60,61 Metallic wires provide radial expansion. with benign biliary strictures have life expectancies that
Because these stents are covered with an impermeable far exceed the expected bare metallic stent patency, use of
membrane, particular care must be taken not to cover these bare stents has been judged to be inappropriate
and potentially occlude the pancreatic duct (risk of pan- when alternative therapies are feasible.3,57
creatitis), the cystic duct (risk of cholecystitis), or a bile Recently, placement of covered bilary self-expanding
duct branch (risk of biliary obstruction, cholangitis, and metallic stents followed by stent retrieval after 2 to
cholangitic abscesses). Long-term biostability of the 6 weeks has been reported to result in a primary patency
fabric membrane is not known. rate of 90.6% and a secondary patency rate of 97% with
a mean clinical and imaging follow-up of 27.9 months.73
These results are preliminary and need to be replicated
Results and Complications by other centers.
After internal-external PBD has been established, the
initial technical success rates for balloon cholangioplasty
are typically high (88% to 100%). Complication rates vary TREATMENT OF MALIGNANT BILIARY
widely (as high as 60%) and usually are caused by sup- STRICTURES (ONLINE CASE 16)
purative cholangitis.* Long-term patency rates depend
on the location and cause of the stricture. Mueller and
Patient and Stent Selection
colleagues64 reported 36-month clinical primary patency
rates of 76% for iatrogenic strictures, 67% for biliary- Expandable metallic stents usually are indicated in long-
enteric anastomotic strictures, and 42% for strictures term patients with malignant strictures, because the stent
caused by sclerosing cholangitis. For patients who have is likely to remain patent for a longer period (median pa-
developed biliary strictures (usually intrahepatic) after tency, 6 to 8 months) than most patients life expectancies
liver transplantation, a 6-year secondary patency of 70% (mean, 3.4 to 7.8 months, depending on tumor type)3,54,72,73
was by reported Zajko and colleagues.53 However, Dia- (Fig. 22-26). Multiple investigators have found that metal-
mond and associates51 observed recurrence in all patients. lic expandable stents remain patent longer, have lower
In patients with transplanted livers, primary patency is complication rates, and require fewer repeat interven-
longer for nonanastomotic strictures than for anastomotic tional procedures to maintain patency compared with
strictures.20,53 Citron and Martin68 reported primary clini- plastic endoprostheses, particularly those delivered
cal patency rates (mean follow-up, 32 months) of 100% for through the transhepatic route.75-77 Metallic stents with a
intrahepatic CBD strictures; 92% for extrahepatic, extra- relatively tight lattice such as the Wallstent (Boston Scien-
pancreatic CBD strictures; 33% for intrapancreatic stric- tific) or the Strecker nitinol stent (Boston Scientific), and
tures; and 75% for biliary-enteric anastomotic strictures. stents that are significantly longer than the diseased
Cantwell69 reported clinically significant restenosis rates segment provide optimized patency, because they resist
following balloon cholangioplasty for treatment of be- tumor ingrowth through the stent struts and are less
nign postoperative biliary strictures of 48% at 5 years and prone to tumor overgrowth beyond the ends of the stent.
59% at 25 years. Restenosis rates were significantly higher Covered stents such as the Viabil stent (WL Gore Inc.,
in patients who underwent repeated dilations. Most in- Flagstaff, Ariz.) may improve primary patency because
vestigators leave 10- to 14-Fr (3.3- to 4.7-mm) soft cathe- the impermeable fabric prevents tumor ingrowth into the
ters across the cholangioplasty site for several weeks or stent lumen.60,61 Krokidis and colleagues78 demonstrated
months to act as a stent, although the need for postdila- less stent dysfunction and improved overall survival in
tion catheter stenting is undocumented. patients with malignant extrahepatic bilary obstructions
Reported technical success and clinical response for treated with covered Viabil stents compared to those
use of metallic expandable stents to treat benign biliary treated with bare Wallstents.
strictures approaches 100%. The rate of major nonfatal
complications is 5% to 18%, although only one procedure-
Results and Complications
related fatality occurred among 174 patients so treated.
Reported initial technical success rates range from
*See references 15, 20, 48-50, 53, 62-69. 75% to 100%.56,72,79 Initial clinical relief of symptoms oc-
See references 50-52, 56-58, 71, 72. curs in greater than 70% of patients.56,72,74,79-86 Reported
22. BILIARY SYSTEM 675
A B
C D
FIGURE 22-26 Expandable metallic stent for treatment of malignant stricture (hilar cholangiocarcinoma). Computed tomography (not
shown) identified bilateral bile duct dilation. A, Transhepatic cholangiography through a left-sided approach documents hilar common bile
duct (CBD) occlusion and mass (arrows). B, An angiographic catheter has been negotiated across the occlusive tumor into the CBD. C, Two
10-mmdiameter, 90-mmlong Wallstents (curved arrows) have been deployed from separate left- and right-sided biliary accesses to drain both
biliary systems. Temporary external-type drainage catheters (straight arrows) have been left to provide overnight external biliary decompression
to minimize the risk of cholangitis or sepsis and to provide transhepatic biliary access while the external drains are capped during a trial of
internal drainage. The external biliary drains usually are removed after 1 to 2 days if internal drainage is successful. D, Cholangiogram
performed through the external drains documents satisfactory stent placement and free drainage into the duodenum.
procedure-related fatality rates range up to 3%. Major report improved primary patency results at 6 months
nonfatal periprocedure complications range from 8% to (76%, 77%) and 12 months (76%, 77%) using covered
61% and are related primarily to the initial establish- stents to treat malignant strictures, although mean
ment of PBD rather than the additional deployment of survival remained short (146 days and 9.2 months).60,61
a metallic stent. The incidence of cholecystitis (12%) and branch duct
Reported primary patency rates of bare stents range obstruction (10%) was higher than expected with bare
from 67% to 85% at 6 months, 50% to 55% at 1 year, and metallic stents. The cost of the covered stents is ap-
10% to 37% at 2 years. Given the relatively short life proximately two to three times that of most bare
expectancies of these patients, only about 7% to 29% of metallic stents, although total cost was equivalent in
stents require reintervention. Thirty-day mortality the Krokidis study.78
rates are approximately 10% to 15%, and death results For percutaneous brachytherapy, the internal-external
primarily from the underlying malignancy. Several in- PBD catheters make ideal conduits for passage of iridium
vestigators are studying coated and impregnated stents Ir-192 wires or seeds incorporated into a modified angio-
to preserve conduit patency.60,61,87-89 Some investigators graphic guidewire. This treatment is useful particularly
676 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
for locally invasive Klatskin-type cholangiocarcinomas of sinus tract may require multiple sessions, particularly if
the porta hepatis. A thin platinum shield absorbs beta the stones are numerous, large, or impacted in intrahe-
particle emission, resulting in local intraductal delivery of patic bile ducts located peripheral to biliary strictures.
pure gamma radiation. Brachytherapy may be combined In patients with innumerable biliary calculi (e.g.,
with external beam irradiation. Although this treatment is recurrent pyogenic cholangitis), large stones ("1.5 cm
not commonly used, several reports suggest modest sur- diameter), or unfavorable anatomy (e.g., prior biliary-
vival improvement (i.e., 10 to 17 months vs. 2 to 8 months enteric drainage procedure), stone removal may be
for historical controls treated with PBD and no irradia- performed by a percutaneous transhepatic route (see
tion).90-94 Infectious and hemorrhagic complications are Fig. 22-11). Although some cases may be managed with
common in this group of patients with or without irradia- fluoroscopically guided techniques similar to those em-
tion; however, ulceration of the gastrointestinal tract is an ployed for stone extraction through a T-tube sinus tract,
added risk of radiation therapy.90 After irradiation, de- many of these patients have such a large stone burden or
ployment of expandable metallic stents may provide im- complex biliary anatomy (dilated and strictured) that
proved biliary drainage with a lower rate of infectious percutaneous endoscopically guided lithotripsy tech-
complications and possibly longer survival.57,94 niques are required for successful therapy.107-109
Between 4 and 10 days after biliary drainage has been
established and cholangitis or sepsis has been treated, the
TREATMENT OF BILIARY STONES transhepatic tract is dilated to accommodate a large (e.g.,
(ONLINE CASES 41 AND 63) 18-Fr) sheath. A small-bore endoscope (e.g., 15-Fr choledo-
choscope with a 6-Fr working channel) is advanced through
As an alternative to operative removal, endoscopic sphinc- the sheath into the biliary system, directed to the stones,
terotomy followed by biliary stone extraction using wire and used to guide stone fragmentation with a suitable
retrieval baskets or occlusion balloons often is used in lithotriptor (e.g., electrohydraulic lithotriptor, ultrasonic
patients with retained CBD stones after cholecystectomy. lithotriptor, pulsed-dye laser). Care must be taken to avoid
It is used also for patients with choledocholithiasis and an the surrounding bile duct walls or subjacent blood vessels.
intact gallbladder who are older than 65 years or are at Reported technical success for percutaneous transhe-
high risk for operative CBD exploration. The procedure patic lithotripsy ranges from 93% to 100%, although
is associated with a high rate of technical success (i.e., suc- complications can be substantial; procedure-related fa-
cessful sphincterotomy in approximately 95% in current tality rates are 0% to 4%, and nonfatal major morbidity
series, with clearance of stones in approximately 85%).95-102 rates are 0% to 24%.107-112 Patients with large stones or
The morbidity rate of approximately 4% to 16% is rela- innumerable stones are likely to have recurrent calculi
tively low. Major complications usually are caused by even if the biliary tracts appear stone free, especially
hemorrhage from the sphincterotomy, pancreatitis, sepsis, when strictures are present. Transhepatic endoscopy
or bowel perforation. also has been used for staging and biopsy in patients
A mature T-tube sinus tract (at least 5 weeks old) can with suspected cholangiocarcinoma, differentiation of
be used for stone extraction (Fig. 22-27). A guidewire is cholangiographic masses or filling defects, removal of
placed through the T-tube, and the T-tube is removed and postoperative biliary foreign bodies (e.g., sutures or
replaced with a sheath, which is directed toward the stone. clips), guidance for cauterization of intraductal bleeding
The guidewire is withdrawn and replaced with a wire sites, and inspection of biliary-enteric anastomoses.*
basket (e.g., Wittich or Dormia Stone basket [Cook Inc.]).
The expanded diameter of the basket varies and should be
selected to match the diameter of the bile duct. The basket BILIARY LEAKS
is opened by withdrawing a protective sheath. The stone
is entrapped by spinning the basket, after which the Biliary leaks usually result from biliary tract surgery.
sheath is gently snuggled down over the basket. Suffi- Other causes include hepatic surgery or invasive proce-
ciently small stones may be removed through the T-tube dures, ischemia due to hepatic arterial occlusive disease
sinus tract. Otherwise, a balloon occlusion catheter can be (e.g., liver transplant recipients), downstream biliary ob-
used to deliver intrahepatic calculi into the CBD and then struction, or penetrating injuries (see Fig. 22-18). Because
to push them into the bowel (see Fig. 22-27). At the end of bile can escape into the peritoneum or a localized space,
the procedure, a drainage catheter is left in place to mini- the intrahepatic bile ducts usually are not dilated. The
mize the likelihood of sepsis, provide a route for follow-up diagnosis and characterization of the biliary injury re-
cholangiography, and preserve access in case some stones quire cross-sectional imaging, preferably with computed
remain. Technical success rates in experienced hands tomography (CT), to assess for bilomas or abscesses,
range from 77% to 97%, with major complications in 4% to and cholangiography with or without endoscopy.
9% of cases and procedure-related fatality rates of 0 to
1%.102-106 Percutaneous stone extraction through a T-tube *See references 26, 39, 109, 110, 113, 114.
22. BILIARY SYSTEM 677
A B C
D E
FIGURE 22-27 Endoscopic, operative, and percutaneous T-tube treatment of biliary calculi. A, Endoscopic retrograde cholangiopancrea-
tography shows multiple common bile duct (CBD) and intrahepatic biliary stones (straight arrows). The sphincterotome (curved arrows) was
used to perform a papillotomy; multiple CBD calculi were removed using wire stone retrieval baskets and an occlusion balloon catheter.
B, One week after an operative cholecystectomy for cholecystolithiasis and CBD exploration, the T-tube cholangiogram detected a retained
7-mmdiameter stone in the distal CBD (curved arrow) and a weblike stricture of the central left bile duct (straight arrow). C, After passage of
a heavy guidewire, the T-tube was replaced with a 12-Fr vascular-type sheath (open arrows). A 10-mm # 4-cm balloon dilation catheter (solid
arrows) was used to dilate the left bile duct stricture. D, An occlusion balloon (arrow) was used to push the stone into the CBD and through
the papilla into the duodenum. E, A completion cholangiogram confirmed the stones absence.
required for exposure of the bile ducts or vascular struc- this diagnosis include abnormal liver function test results,
tures is reduced significantly.123 PBD also may assist intra- right upper quadrant pain, and sonographic findings
operative placement of transhepatic Silastic biliary stents of a distended gallbladder, thickened gallbladder wall,
or U-tube drains (Silastic tubes placed across a stricture or intraluminal sludge or stones, pericholecystic fluid, or the
anastomosis, one end externalized through the liver and presence of a sonographic Murphys sign. Radionuclide
the other end externalized through an enterotomy). studies are of little value, because most critically ill
In patients in whom endoscopic drainage has failed patients do not show radionuclide uptake by the gallblad-
because of inability of the endoscopist to cannulate the der on hepatobiliary scintigraphy. The diagnosis is based
bile ducts, the so-called rendezvous procedure may be on the clinical response to percutaneous cholecystostomy
performed to permit endoscopic access into the biliary because neither the Gram stain nor the results of bile
systems or to provide improved guidewire tension for culture are helpful.127
delivery of transluminal devices across difficult stric- The second indication is calculus cholecystitis in poor
tures.124,125 The rendezvous procedure is performed by operative candidates (Fig. 22-29). In patients whose opera-
passing a 300- to 400-cm guidewire and 5- to 6-Fr an- tive contraindication is temporary (e.g., acute myocardial
giographic catheter percutaneously through the biliary infarction), percutaneous cholecystostomy permits drain-
system and into the small bowel. The endoscopist then age of the gallbladder so that cholecystectomy may be
can snare the guidewire easily and withdraw it through performed electively at a later time. In patients with a per-
the mouth. The through-and-through body floss manent contraindication to surgery (e.g., intractable con-
guidewire is threaded through the working channel of gestive heart failure), the percutaneous cholecystostomy
the interventional endoscope, and the desired translu- access route can be used to extract the gallstones using
minal device (e.g., endoprostheses and pusher catheter, forceps, wire baskets, or various lithotriptors.128 In ap-
expandable metallic stent delivery system) is passed proximately one half of patients, gallstones do not recur.129
over the guidewire retrograde into the desired location
in the biliary system. After the guidewire is removed,
Technique
the angiographic catheter may be used for antegrade
cholangiography and as a safety drain in case of infec- Percutaneous cholecystostomy may be performed at
tious complications or unexpected biliary obstruction. the bedside under sonographic guidance in critically
The primary advantage of the rendezvous proce- ill patients. When feasible, the procedure should be
dure is the ability to place a relatively large-bore drain performed in an interventional radiology suite to per-
(3.3 to 12 mm) with a small-caliber transhepatic route mit manipulation of guidewires and catheters under
(1.7 to 2 mm). However, expandable metallic stents often fluoroscopy. In patients with distorted anatomy, CT
can be placed more simply by a transhepatic approach. may be necessary to obtain initial skinny-needle and
Rendezvous procedures now are used less frequently guidewire access into the gallbladder.
than in the past. Two percutaneous approaches may be used for cho-
lecystostomy. In the transhepatic approach, a needle is
directed from a subcostal or intercostal site in the right
PERCUTANEOUS CHOLECYSTOSTOMY mid-axillary line toward the bare area of the gallblad-
(ONLINE CASE 9) der fossa, where the gallbladder is attached to the liver
capsule. The primary advantages of this route are that
the likelihood of bile spillage into the peritoneum is
Patient Selection minimized and the gallbladder is relatively fixed to
Most benign disease of the gallbladder is managed by the liver, which facilitates puncture of the gallbladder
operative cholecystectomy. During the late 1980s and wall. Disadvantages include the risk of hemorrhagic
early 1990s, several nonoperative techniques were complications from transhepatic passage and the
developed as an alternative to open cholecystectomy 90-degree angle with the long axis of the gallbladder,
for treatment of calculus cholecystitis, including percu- which makes catheter manipulations difficult.
taneous cholecystostomy with percutaneous lithotripsy In the transperitoneal approach, the needle is directed
or stone dissolution and extracorporeal shock wave from the subcostal right anterior abdomen, beneath the
lithothripsy.126 The rapid growth of laparoscopic chole- liver margin into the fundus of the gallbladder along the
cystectomy during the early 1990s has largely rendered long axis of the organ. This technique is safest in patients
these techniques obsolete. with a distended gallbladder, which is often adherent
There are two major indications for percutaneous to the anterior abdominal wall (see Fig. 22-28). Advan-
cholecystostomy.6 The first is possible acalculous cholecys- tages of transperitoneal access include avoidance of the
titis in critically ill patients with sepsis of unknown origin hemorrhagic complications associated with the transhe-
(Fig. 22-28). In septic patients, clinical features suggesting patic route and pain from intercostal catheter passage
22. BILIARY SYSTEM 679
C D
A B
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C H A P T E R
23
Urologic and Genital Systems
Matthew Kogut, Todd L. Kooy, Steven B. Oglevie
Genitourinary interventional radiology has evolved renal pelvic punctures also risk the formation of a uri-
with the advances in knowledge and technology. With noma after the tube is removed.
vast improvements in the diagnostic capabilities of non- The calyces are usually arranged in anterior and pos-
invasive imaging, purely diagnostic catheter-based im- terior rows. At the upper and lower poles, fusion can
aging studies are performed infrequently. Although result in compound calyces. During urography in the
many of the genitourinary interventions have been per- anteroposterior projection, classic teaching is that poste-
formed for decades, the procedures have been refined rior calyces are located medially and seen en face, while
with new equipment and continuous improvements in anterior calyces are located more laterally and seen in
imaging guidance. Various percutaneous drainage pro- profile. However, a recent evaluation of calyceal anat-
cedures involving the urinary collecting system remain omy on computed tomography (CT) showed that this is
necessary tools for the interventionalist. However, col- not the case in the lower pole. Most lower poles have
laboration with urologists, transplant surgeons, obstetri- two to three calyces and the most posterior calyx was
cians, and gynecologists has also allowed us to hone often more lateral.1 However, normal variation occurs,
advanced techniques and expand into new areas such as which is why, with the patient in prone position, oblique
renal transplant interventions and transcervical steril- imaging, ultrasound, or injection of air is recommended
ization via fallopian tube occlusion. to identify posterior calyces. Discrimination between
the anterior and posterior calyces is critical, because
posterior calyces are strongly preferred for most PCN
PERCUTANEOUS NEPHROSTOMY procedures.
(ONLINE CASES 24 AND 36) Understanding the normal and variant relationships
of the kidneys with surrounding structures is important
for safe and successful placement of a PCN.2 The de-
Anatomy scending colon lies in the anterior pararenal space, and
The kidneys are retroperitoneal organs surrounded by its relationship to the left kidney is determined by the
perinephric fat and enclosed by Gerota fascia. Their axes position of the lateroconal fascia. In approximately 10%
parallel the psoas muscle so that the upper pole is me- of patients, the descending colon lies behind a horizontal
dial and slightly more posterior than the lower pole. line at the posterior edge of the left kidney. In about 1%
During normal development, the kidney ascends and of cases, the descending colon extends behind the left
rotates medially about its vertical axis such that the renal kidney.3 Rarely, the ascending colon lies posterolateral to
hilum is directed anteromedially at an angle of approxi- the right kidney and medial to the liver.
mately 30 degrees from the horizontal plane. The pleura extends posteriorly down to the 12th ver-
The main renal artery and vein lie anterior to the re- tebral body and then extends laterally, crossing the
nal pelvis. However, a posterior branch of the renal ar- 12th, 11th, and 10th ribs. Although great normal varia-
tery courses behind the renal pelvis to supply the dorsal tion occurs, about one half of the right kidney and one
segments. A percutaneous nephrostomy (PCN) track third of the left kidney lie above this posterior reflection
extending directly into a calyx has the least chance of of the pleura.
causing substantial arterial injury (Fig. 23-1). Punctures The liver is anterolateral to the upper pole of the
into an infundibulum or directly into the renal pelvis right kidney. In some patients, a portion of the right lobe
carry a higher risk of hemorrhagic complications, be- of the liver may extend posterolaterally to the upper
cause larger arterial branches may be traversed. Direct pole of the kidney. The position of the spleen is more
684
23. UROLOGIC AND GENITAL SYSTEMS 685
BOX 23-1
I N D I C AT I O N S
F O R P E R C U TA N E O U S
NEPHROSTOMY
Patient Selection
The indications for PCN fall into four broad categories disseminated malignancies and very short life expec-
(Box 23-1). Each patient must be considered individu- tancies, decompression may not be indicated. Many
ally, because some have both indications for and contra- oncologists believe a uremic death is a reasonably pain-
indications to the procedure. The decision about whether less way for a terminal patient to die. This decision must
to perform PCN depends on the details of the particular be addressed individually and tailored to the desires of
situation and on the other available options. the patient and his or her family.
In patients with acute unilateral ureteral obstruction,
Relief of Urinary Obstruction decompression is justified to preserve renal function on
The most common indication for PCN is relief of uri- the affected side. Long-standing obstruction is associated
nary obstruction. Imaging studies should be performed with an irreversible deterioration of renal function and
to demonstrate dilated collecting systems, and they parenchymal atrophy. Although the patients serum
usually delineate the anatomic level of obstruction and blood urea nitrogen and creatinine levels usually do not
the cause. The ureteral obstruction may be acute, as become elevated with unilateral obstruction, the damage
with obstructing ureteral calculi or traumatic ureteral to the ipsilateral kidney is progressive and irreversible
injury. However, the obstruction may be long-standing, when not addressed promptly. Decompression with PCN
as with primary urothelial neoplasms, extrinsic com- may allow the cause of acute ureteral obstruction to be
pression, or direct invasion by retroperitoneal or pelvic addressed on a more elective basis without risk of losing
malignancies. renal function.
In patients with bilateral obstruction or with obstruc- In any patient with obstruction and suspicion of in-
tion of a solitary kidney, PCN is indicated for preserva- fection, emergent decompression is indicated. Infection
tion of renal function. In some patients with widely may be suggested by fever, leukocytosis, flank pain, or
686 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
sepsis. These patients must also be treated immediately after a PCN. In fact, decompressive PCN may be indi-
with appropriate intravenous (IV) antibiotics and hemo- cated to assess the recoverable function of a chronically
dynamic support as needed. The decompressive proce- occluded kidney.
dures in patients with pyonephrosis must be conducted
and monitored with care, because the septic condition Diversion of Urine
may be worsened with the intervention. PCN is used to divert urine in cases of urinary leakage
Patients with chronic unilateral hydroureteronephro- (Fig. 23-2). PCN, usually in combination with ureteral
sis due to malignancy do not necessarily require decom- stent placement, allows most ureteral injuries to seal.
pression unless infection is suspected. In the absence of The stent is thought to serve as a scaffold for ureteral
malignant disease, kidneys with an estimated reno- healing. Percutaneous drainage of associated urinomas
graphic glomerular filtration rate (GFR) of greater than that accumulated before urinary diversion also may be
10 mL/min/1.73 m2 will likely stabilize or improve re- performed. In cases of malignant or inflammatory fis-
nal function, while kidneys with worse function may tulas, PCN is indicated to divert urine in conjunction
not be worth salvage.4 The finding of mild or moderate with stent placement. PCN has been used also to divert
cortical atrophy on CT or ultrasound is not a reliable urine and treat patients successfully with hemorrhagic
predictor of limited potential for functional recovery cystitis.5
B
FIGURE 23-2 Decompression of a duplicated collecting system to assist in healing an anastomotic leak between the ureters and
neobladder. A, Computed tomography shows the duplicated ureters near the anastomosis (circle) adjacent to dilute contrast seen in a large
urinoma (arrowhead). The neobladder (arrow) opacified with contrast is partially seen. B, A percutaneous nephrostomy has already been
placed into the upper pole moiety (arrow). Access has been gained to a posterior calyx (arrowheads) in the lower pole. The calyx is outlined
by air, which was injected to confirm a posterior location. C, The upper moiety is now decompressed (arrowheads). The more inferior
nephrostomy was injected with contrast to confirm appropriate location, with the pigtail now formed in the lower moiety renal pelvis (arrow).
23. UROLOGIC AND GENITAL SYSTEMS 687
Access for Diagnostic Interventions Access provided for stone treatment is one of the
Percutaneous access may be performed to permit ante- most common indications for PCN placement. By the
grade pyelography. However, advances in diagnostic age of 70 years, 11% of men and 5.6% of women will
radiology dominated by CT and magnetic resonance have a symptomatic urinary tract stone.11 Although stones
(MR) urography have rendered this indication extremely smaller than 5 mm often pass without intervention,
rare.6 Biopsies of urothelial lesions may be performed stones between 5 and 10 mm have variable outcomes,
through nephrostomy access using brushes and forceps. and stones larger than 10 mm will not pass without in-
Nephrostomy access may be used for diagnostic neph- tervention.11 Many renal calculi can be managed suc-
roscopy and ureteroscopy. Functional studies (e.g., Whitaker cessfully with extracorporeal shock wave lithotripsy
test) can be performed to determine the significance of (ESWL) or percutaneous nephrostolithotomy (PCNL),
urographically detected stenoses and to assess the re- with success rates that rival open surgery but with sig-
sults of interventions such as endopyelotomy or balloon nificantly less morbidity, recovery time, and cost.
ureteral dilation. This procedure is typically reserved for Planning the approach and entry site is the most critical
complicated cases in which nuclear scintigraphy or MR step of the PCNL procedure and should be made by
urography fail to give adequate physiologic information.7 consultation between the urologist and interventional
MR urography may become the one-stop shop for radiologist. The puncture site must allow the stone to be
anatomic and functional information regarding the accessed and removed but not be made directly into the
genitourinary system. pelvis or infundibulum. This is one of the situations where
occasionally supracostal access and/or access to an ante-
Access for Therapeutic Interventions rior calyx is optimal for future treatment (Fig. 23-4). If the
Ureteral strictures may be dilated percutaneously, and initial puncture site is not ideal, it is better to make a new
ureteral stents can also be placed. Foreign bodies (e.g., puncture in a more suitable position than to proceed with
encrusted or occluded ureteral stents) may be retrieved track dilation through which the stone cannot be removed.
through the nephrostomy access (Fig. 23-3). Stone ther- The best approach depends on several factors, the most
apy can be performed by chemodissolution or mechan- important of which is the location of the stone burden.
ical fragmentation and extraction. Antifungal agents
may be infused directly through the nephrostomy
Contraindications
tube to treat fungus balls in the upper urinary tract.8,9
Nephroscopically guided operations can be performed, Contraindications to PCN include uncorrectable coagu-
including resection of urothelial neoplasms and en- lopathy and an uncooperative patient. If hyperkalemia
dopyelotomy. Intracavitary adjuvant chemotherapy can be is severe (i.e., potassium level greater than 7 mEq/L),
administered through a nephrostomy in certain cases of hemodialysis should be performed to correct the electro-
transitional cell carcinoma.10 lyte balance before the procedure.
A B
688 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
C D
FIGURE 23-4 Access for percutaneous nephrolithotomy (PCNL). After consultation with the urologist, the best approach was deemed to
be supracostal and lateral, targeting an anterior midpole calyx containing a stone. A, Initial fluoroscopic guided puncture directed at the mid-
pole stone (arrow). B, A DynaCT was performed on the fluoroscopic table after initial puncture to confirm a safe approach into the calyx that
avoided the colon. An arrowhead shows the supracostal approach and the arrow indicates the fat plane between the track and colon. C, Access
was confirmed to be along the course of the stone (arrowhead) and a 0.018-inch wire (arrows) is coiled in the renal pelvis around the larger stone.
D, Final spot image shows the nephrostomy pigtail formed in the superior aspect of the renal pelvis. A 5-Fr angled catheter (arrowheads) also
traverses the stone down the ureter, terminating in the bladder. This ureteral catheter provides stable access for the urologist.
Surgical and Medical Alternatives during open surgery directly into the renal pelvis, but
It usually is advantageous to initially consider a retro- this is rarely indicated because PCN can be performed
grade approach for renal drainage in patients with ob- safely and effectively in almost all patients (Fig. 23-5).
structive uropathy. PCN is typically reserved for patients Medical therapy for obstructive uropathy is limited. In
in whom retrograde attempts are unsuccessful or not some patients with widely disseminated malignancy
feasible. Although retrograde stents need routine changes or retroperitoneal fibrosis and obstructive uropathy, re-
and management, the patient will not have an external nal function may improve with the administration of
tube to manage. A surgical nephrostomy may be placed corticosteroids.12,13
23. UROLOGIC AND GENITAL SYSTEMS 689
A B C
D E
FIGURE 23-8 Stepwise placement of a decompressive nephrostomy. A retrograde stent is in position, which was not adequately
decompressing the system. A and B, Two different obliquities show puncture of a posterior lower pole calyx, outlined by injected air
(arrowheads). The 22-gauge needle (arrow) has been connected to tubing for injection with continuous fluoroscopic observation. A 0.018-inch
wire was advanced through the collecting system. C, The coaxial set (arrowhead) has been advanced over the 0.018-inch wire, which has been
removed and a stiffer 0.035-inch wire (arrow) has been advanced down the ureter. D, The nephrostomy tube (arrowhead) has been advanced
down the ureter over the wire. E, The nephrostomy tube has been partially withdrawn and the pigtail has been formed in the renal pelvis.
generally are preferred over other self-retaining catheters tomy tube, giving the urologist a stable access for a stiff
(e.g., Malecot, accordion, Foley). The nonpigtail catheters working wire as well as access to the renal pelvis from
occasionally may be useful in collecting systems not the nephrostomy tube.
capacious enough to accommodate a pigtail. In patients The catheter is secured to the skin using adhesive
for whom access was provided for PCNL, a 5-Fr cathe- dressings or suture. Adhesive dressings minimize cath-
ter is often left in the bladder alongside the nephros- eter kinking and reduce the risk of catheter dislodgment.
692 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
Catheter Maintenance
Chronic indwelling nephrostomy tubes usually should
be exchanged every 3 to 6 months to prevent encrusta-
tion and occlusion. Some patients may require exchanges
as often as every 6 weeks. It is better to err on the side of
frequent catheter exchanges than to have the catheter
FIGURE 23-9 Initial puncture (arrowheads) was into an occlude and have the patient develop sepsis or further
infundibulum. This needle was left in place to inject contrast/air deterioration of renal function due to obstruction. If the
to guide a second needle into a lower pole calyx. A needle driver catheter is initially exchanged at 3 months and appears
(arrow) is placed on the patient to mark the proposed skin entrance
site. A small amount of extravasation is seen.
to be functioning well, the interval may be increased by
1 month at a time for up to 6 months.
Colonization with bacteria, fungi, or both invariably
develops in patients with chronic indwelling nephros-
tomy tubes.18 Asymptomatic bacteremia occurs fre-
quently (about 10% of the time) during routine catheter
exchanges; preprocedural antibiotics are not successful
at preventing bacteremia.19 Nonetheless, some operators
routinely give antibiotics for tube exchanges, particu-
larly when the tube has been functioning poorly. For
patients with cardiac valvular disease, a full course of
antibiotics should be administered before catheter ex-
change to minimize the risk of bacteremia. Despite
therapeutic levels of antibiotics during catheter ex-
change, a septic reaction may still occur as a reaction to
endotoxin released into the vascular system.
Patients with occluded catheters can present a chal-
lenge for catheter exchange. The pigtail catheter reten-
tion string initially should be secured so that it is not
pushed down the catheter into an occlusive tangle with
repeated attempts at guidewire passage. Hydrophilic
guidewires are preferred for negotiating an occluded
catheter. If the endhole cannot be passed, a side hole is
acceptable. After the guidewire is through the catheter,
FIGURE 23-10 The patient needed a nephrostomy for treatment the string is released to allow the loop to open. If no
of a lower pole stone not well seen on this image. Urology requested guidewire can be passed, a sheath may be passed over
superior pole access. The outer dilator of the coaxial set is at the access
the catheter, after its hub has been cut off. The catheter
point in the posterior superior pole calyx, which is outlined by injected
air (arrow). Given the steep angle of entry to the renal pelvis, an angled can then be removed and replaced through the sheath.
catheter (arrowhead) was necessary to guide the 0.035-inch wire into a Catheter dislodgment represents an urgent situation,
more stable position before placement of the nephrostomy. because rapid tube replacement is required to maintain
track patency. Tracks that have not had a tube replaced
After the track has matured, a simple dry dressing may within 48 to 72 hours are difficult to renegotiate. All pa-
be placed over the exit site. The catheter is left to gravity tients with PCN tubes should be educated about the
drainage with close monitoring of urine output. It typi- urgency of this situation. After sterile preparation, the
cally requires irrigation only if blood clots occlude track is probed with an angled 5-Fr catheter. Contrast
the tube. may be injected to define the track, and a hydrophilic
23. UROLOGIC AND GENITAL SYSTEMS 693
wire and/or the angled catheter is then negotiated back function. Unfortunately, the median survival rate of
into the collecting system. patients with advanced malignant urinary obstruction is
3 to 7 months.27 Even with careful patient selection, 32%
Results of patients are unable to achieve any improvement in
In patients with obstructed, dilated collecting systems, a quality of life after PCN.28 After an open and frank discus-
decompressive PCN can be placed successfully in al- sion about the physical, emotional, and financial burdens
most all cases. Technical success should be expected in associated with a drainage catheter, most patients and
greater than 95% of cases.20,21 In nondilated collecting families opt for the drainage catheter as a means to extend
systems or complex stone cases, technical success may life for as little as a few months.
decrease to 85% or less.
The clinical response to PCN by patients with urosepsis Complications
often is dramatic. In one series of patients with gram- The mortality rate for PCN is about 0.2%, which com-
negative septicemia and urinary obstruction complicated pares favorably with the mortality rate for surgical
by infection, PCN reduced mortality from 40% to 8%.22 nephrostomy (!6%).20 The major procedure-related
However, PCN in patients with pyonephrosis may exacer- complications are bleeding and sepsis. Hemorrhage re-
bate or precipitate septicemia as a result of bacteria enter- quiring transfusion or other treatment occurs in 1% to
ing the bloodstream through peripapillary veins from 3% of patients undergoing PCN.20 One series of 144
catheter manipulation or overdistention.22,23 nephrostomies placed using combined CT and fluoro-
In patients with fungal urinary infections, antifungal scopic guidance had no hemorrhagic or other major
agents can be infused directly into the collecting system. complications.29 Most bleeding associated with PCN is
This approach is advantageous because effective thera- transient and self-limited. It is not uncommon to have
peutic levels can be achieved in the urinary tract without pink urine for several days after the procedure. If small
the associated systemic toxicity from IV administration. clots block the catheter, the catheter should be irrigated
Fungus balls can be disrupted mechanically and extracted with sterile saline.
through the nephrostomy tract.8,24 Major arterial injury should be suspected when the
In most patients with azotemia due to obstruction, urine remains grossly bloody after 3 to 5 days, when
PCN provides rapid improvement of renal function.25 The new clots are demonstrated in the collecting system on
procedure commonly is used as a temporizing measure to follow-up nephrostograms, or when there is a signifi-
improve renal function while the underlying obstruction cant drop in hematocrit. These patients should undergo
is addressed definitively. In patients with terminal malig- angiographic evaluation with embolization of injured
nancies and azotemia due to bilateral obstruction, unilat- vessels (Fig. 23-11). If the initial angiogram is negative,
eral PCN usually suffices to preserve renal function.26 the nephrostomy may be removed over a guidewire to
Bilateral drainage is indicated if pyonephrosis is suspected relieve the tamponading effect of the catheter, and the
or unilateral drainage is unsatisfactory for restoring renal angiogram is repeated. If the drop in hematocrit is out of
A B C
FIGURE 23-11 Arterial injury from percutaneous nephrostomy. The patient had persistent bright red hematuria after removal of a
lower pole nephrostomy. A, Selective left renal artery angiography shows active extravasation (arrow) from a lower pole branch in the previ-
ous location of the nephrostomy tube. B, A 3-Fr microcatheter (arrowhead) has been advanced to the distal aspect of the offending branch
and injection shows extravasation (arrow). C, Angiography from the microcatheter (arrowhead) after coil embolization (arrow) shows reflux
into normal renal artery branches and occlusion of the previously bleeding lower pole branch.
694 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
proportion to the quantity of blood in the urine, the pa- along the nephrostomy track. These complications are
tient may have a retroperitoneal hematoma. Retroperito- prevented by obtaining access beneath the 12th rib. One
neal hemorrhage is best evaluated with CT. Unsuspected study showed that PCN tracks above the 12th rib tra-
retroperitoneal hematomas not requiring treatment have verse the pleura in 29% of cases on the right and 14% of
been reported in up to 13% of patients.30 Significant cases on the left.33 Pleural complications occur in only
hemorrhage usually is caused by laceration of lobar about 0.2% of decompressive nephrostomies.21 When
arteries. Pseudoaneurysm, arteriovenous fistula, arterio- supracostal access is required for stone therapy, the risk
caliceal fistula, or frank extravasation may be seen at of pleural complications increases to as much as 12%.34,35
arteriography. The risk of hemorrhage is minimized by However, many pleural transgressions remain clinically
using fine needles for puncture, using appropriate guid- silent.
ance, and avoiding puncture of the anteromedial renal Minor perforations of the collecting system occur in
vessels. The vast majority of these complications can be about 2% of patients. If a satisfactory drainage catheter
managed endovascularly.31 is placed in the collecting system, these leaks usually
Although there is always concern for infection in pa- heal spontaneously over the next 48 to 72 hours. The risk
tients with the need for urinary decompression, sepsis only of urine leak as well as hemorrhage is increased with a
occurs in approximately 1% to 3.6% of patients undergoing direct renal pelvis puncture (Fig. 23-12). Urinomas re-
nephrostomy placement (the higher incidence seen in quiring drainage are less common and occur rarely with
patients undergoing decompression for suspected infec- standard 8- to 12-Fr PCN tubes. After removal of larger
tion).32 Patients with infected urine or stones are at higher PCN catheters used for nephrostolithotomy, urinomas
risk for PCN-related sepsis. For elective PCN for stone are more common. Other rare complications of PCN in-
disease, antibiotic therapy ideally should be initiated and clude air embolism and puncture of the colon, spleen,
continued until the urine is clear. Diagnostic nephrosto- liver, and gallbladder.36-39
grams, ureteral catheterization, and stent placement should Catheter dislodgment is a relatively common occur-
be delayed in patients with pyonephrosis until the urine rence. In a recent review of 283 patients with 325 neph-
has cleared. rostomy tubes, there was an episode of complete dis-
Pleural complications include pneumothorax and lodgment of the catheter in 16.6% of the patients. The
empyema from infected urine entering the pleural space vast majority of the tubes were replaced through the
A B
FIGURE 23-12 A, Nephroureteral catheter (arrow) was placed to treat a ureteral stricture. Injection of the catheter shows extravasation
(arrowheads) extending from the pelvis and along the track. B, Computed tomography shows that the catheter (arrowheads) directly enters the
renal pelvis. Extravasated contrast (arrow) is present in the perinephric space along the track.
23. UROLOGIC AND GENITAL SYSTEMS 695
preexisting track, with a limiting factor of track maturity. exchange may be required as frequently as every 6 weeks.
Successful replacement rates were 17%, 35%, and 97% in In general, stents should be exchanged at least every
tracks less than 4 weeks old, less than 6 weeks old, and 6 months with transurethral cystoscopic or fluoroscopic
more than 6 weeks old, respectively.40 Some patients guidance to prevent encrustation and occlusion. Stents
have recurrent dislodgment of their tubes. One author may cause debilitating irritation of the bladder wall or
describes a solution by placement of a renal U-tube. trigone. Some patients prefer externally draining PCN
This tube goes in one polar calyx and out the other pole tubes because function can be assessed easily and re-
with side holes within the collecting system.41 Malecot placement is simple.
catheters commonly used after nephrostomy track dila- The nephroureteral (NU) stent is an alternative to
tion may become difficult to extract if tissue bridges externally draining PCN tubes and internally drain-
grow over the catheter flanges.42 These devices should ing ureteral stents. This device differs from the stan-
therefore be used with caution for long-term drainage. dard double-J ureteral stent in that it has a retention
The entrapped catheters may be safely removed using loop positioned in the renal pelvis and a short seg-
endoscopic techniques to cut the anchoring tissue ment of catheter extending out the nephrostomy track.
bridges. The external segment of catheter may be capped to
restore antegrade flow of urine from the renal pelvis,
through the stent, and into the urinary bladder. The
URETERAL STENT PLACEMENT advantage of this device is that diagnosis of occlusion
requires only a nephrostogram. If the patient devel-
ops flank pain or fever, she or he can open the catheter
Patient Selection to external drainage until receiving medical attention.
Ureteral stent placement is indicated for a broad variety Likewise, catheter exchange over a guidewire is sim-
of clinical problems (Box 23-2). PCN tube placement ple and does not require anesthesia, cystoscopy, or
with antegrade stent placement usually is reserved for other transurethral interventions. These catheters are
patients in whom retrograde attempts are unsuccessful ideal for short-term ureteral stenting when it is ad-
or not feasible. For patients with nephroureteral obstruc- vantageous to maintain access to the upper urinary
tion, ureteral stents have distinct advantages over exter- tract for further evaluation with nephrostograms or a
nal drainage through a PCN tube. The drainage with Whitaker test.
stents is internalized, eliminating the need for external External PCN drainage is preferred over ureteral
drainage tubing and collecting bags. The completely in- stents in several situations, particularly when there are
ternalized ureteral stent is tolerated better by patients, contraindications to ureteral stent placement (Box 23-3).
and it decreases the risk of urosepsis from the inevitable In the occasional patient with vesicocutaneous fistula
colonization of external drainage catheters.43,44 Ureteral due to advanced pelvic malignancy, diversion of urine
stents also have several disadvantages. Stent malfunc- with ureteral occlusion is beneficial to facilitate fistula
tion may not be detected quickly and often requires closure and minimize tissue breakdown and nursing
sonography or cystography for diagnosis. Stent patency care requirements. Nephroureteral catheters are avail-
varies with the clinical situation. Stone-forming pa- able with ureteral occlusion balloons to treat this diffi-
tients tend to develop rapid stent occlusion, and stent cult group of patients.
I N D I C AT I O N S F O R C O N T R A I N D I C AT I O N S
URETERAL STENT TO URETERAL STENT
PLACEMENT PLACEMENT
collecting system, usually in the renal pelvis. The peel- If there is great difficulty advancing catheters over
away sheath is then removed. Holding the pushing cath- the guidewire and through the stricture, the guidewire
eter in place, the stiffener is removed. By gently pulling on may be passed through the urethra to provide through-
the suture attached to the proximal end of the stent, it can and-through access and facilitate catheter passage. A
be positioned in the renal pelvis and the pigtail configura- blunt Foley catheter lubricated with viscous lidocaine
tion formed. This step usually requires withdrawal of the jelly is passed into the bladder. A guidewire then is ad-
stiff guidewire, at least until only the floppy tip remains in vanced through the Foley catheter, which is exchanged
the proximal end of the stent. When the proximal end of for a short vascular sheath to protect the urethra during
the stent is released, the guidewire may be advanced and subsequent interventions. The ureteral guidewire may
coiled in the renal pelvis for subsequent nephrostomy be captured in the bladder using a vascular snare and
placement. Alternatively, the nephrostomy may be placed pulled out through the urethra to provide secure,
over a safety guidewire introduced at the beginning of the through-and-through access.47 With both ends of the
procedure. The suture is cut and removed by pulling wire held securely, a stent can be advanced through
on one end while observing the stent fluoroscopically to almost any stricture.
ensure it remains in optimal position. This technique also has proven useful for replace-
A nephrostomy tube usually is left in place, draining ment of ureteral stents in women (Fig. 23-16). After cap-
externally, for 24 hours (Fig. 23-15). After 2 hours, if he- turing the free end of the stent in the urinary bladder, it
maturia has cleared, the PCN should be capped to force is pulled through the urethra. As soon as the stent tip is
urine through the stent and prevent early stent occlusion brought out of the urethra, a guidewire is advanced up
with clot. If the patient subsequently develops flank pain the stent into the renal pelvis. Stent replacement over the
or fever, the PCN can be opened to gravity drainage. An guidewire is then straightforward. This fluoroscopically
antegrade nephrostogram is performed the day after guided technique is successful in up to 97% of cases.48 It
stent placement to confirm stent location and patency is simple and well tolerated by female patients because
before nephrostomy removal. The nephrostomy should of the short urethra.
be removed under fluoroscopic observation, preferably Patients with urinary diversions into an ileal conduit
over a wire to ensure that it does not become entangled who develop obstruction may be treated with retrograde,
in the ureteral stent or cause trauma as the tip of the loop antegrade, or combined placement of ureteral stents. If
drags against the track wall. contrast refluxes from the conduit into the ureter, the
A B
698 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
C
23. UROLOGIC AND GENITAL SYSTEMS 699
A B
A B C
FIGURE 23-19 Treatment of ureteral occlusion related to prior pelvic surgery. A, The low ureteral stenosis has been crossed, initially
with a glidewire and angled catheter. The glidewire has been exchanged for a stiff guidewire and an 8-mm balloon is inflated at the level of
stenosis. B and C, Following ureteroplasty, a nephroureteral stent was placed (8 Fr) and will remain as a scaffold to urothelial healing for at
least 6 weeks.
Stents of at least 8 to 10 Fr are generally used. If larger patent and there is flow across the lesion into the blad-
catheters are needed or desired, an internal-external der, the NU stent can be replaced with a double-J ure-
biliary catheter with extra proximal side holes can be teral stent and nephrostomy catheter or just a nephros-
placed with the pigtail loop formed in the bladder. After tomy catheter. A trial of capping the nephrostomy tube
6 to 8 weeks, the NU stent is removed over a guidewire is recommended before giving up percutaneous access.
and an antegrade nephrostogram is performed. The If initial trials fail, attempts should be made with either
Whitaker test may also be helpful if there is concern a larger balloon, a cutting balloon with a larger stent, or
for residual obstruction (see later). If the ureter looks possibly with a cryoballoon43,57,58 (Fig. 23-20).
23. UROLOGIC AND GENITAL SYSTEMS 701
A B
C D
FIGURE 23-20 A, A 40-year-old woman with history of anorectal carcinoma and low anterior resection of the colon and rectum with
adjuvant chemotherapy and external beam radiation to the pelvis. She developed ureteral obstruction following external beam radiation
therapy. Despite a trial with double-J ureteral stents, she suffered from recurrent obstruction, urinary tract infection, and urosepsis. Initial
image from antegrade nephrostogram shows occlusion of the ureter (arrow). B, Initial attempt at ureteroplasty performed with a conventional
8-mm balloon after ureteral obstruction was crossed with a glidewire and lesion predilated with a low-profile 4-mm balloon. C, After failing
ureteroplasty with an 8-mm conventional balloon and cutting balloon, an attempt was made with a cryoplasty balloon (arrow). D, Final image
from antegrade nephrostogram following ureteroplasty with 8-mm cryoballoon and 6 weeks of nephroureteral stent placement.
702 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
C D
FIGURE 23-21 Suprapubic catheter placement. A, Typical ultrasound image of the bladder with moderate distention before suprapubic
catheter placement. B, Transurethral Foley catheter placement (arrow) and distention of the bladder with contrast. The anterior bladder wall
has been punctured and a guidewire is in place (curved arrow). C, Typical appearance following suprapubic catheter placement. A midline
approach was used and the retention balloon is seen displacing contrast. D, A Council tip Foley catheter has been placed in the bladder from
a suprapubic approach. A transurethral Foley is also in place, which allows bladder distention and improves visualization during suprapubic
catheter placement.
indicate obstructive uropathy.71 More recent reports and is less likely to be associated with successful intra-
claim that decreasing the pressure gradient threshold uterine pregnancy.79
increases the sensitivity of the exam. These investigators The most common site of tubal occlusion is within the
have proposed using 12 cm H2O gradient as the cutoff proximal, intramural portion of the fallopian tube, which is
for normal, 12 to 18 cm H2O as equivocal, and greater about 1 cm long and has a diameter of approximately
than 18 cm H2O as indicative of obstructive uropathy.74 1 mm. Infection and subsequent inflammation or fibrosis
If the pressure gradient is initially equivocal, increas- are almost always responsible for tubal disease. Gonococ-
ing the perfusion rate (up to 20 mL/min) can help resolve cal and chlamydial salpingitis, postpartum endometritis,
uncertainty and may unmask functional obstruction. spasm, impacted mucus and debris, polyps and synechiae
When the test result is positive, spot films should be are all causes of proximal tubal occlusion. Fallopian tube
obtained to document the site of obstruction. If the chal- occlusion in the isthmic, ampullary, or fimbriated portions
lenge test result is negative or indeterminate, it may be of the tube usually is caused by previous pelvic infection or
helpful to repeat the study with the bladder distended, endometriosis.
because some cases of obstruction are evident only after
bladder filling. Likewise, repeating the challenge with
Patient Selection
the patient in different positions may produce a positive
result.75 HSG and selective salpingography are indicated for
evaluation and possible treatment of women thought to
have infertility related to tubal occlusion, particularly in
Results and Complications the isthmic portion of the tube. Recanalization should be
The accuracy of the ureteral perfusion challenge has not attempted when bilateral proximal tubal occlusion is
been established, in part because there is no gold standard identified on hysterosalpingogram.
against which test results can be compared. Lupton and
colleagues, in a study of 145 patients, found that 61 cases
Technique
showed obstruction, 53 were unobstructed, 4 were equiv-
ocal, 17 showed abnormal peristalsis, and 10 described The procedure is generally performed on an outpatient
loin pain during the test.71 They reported that the Whita- basis and should be scheduled during the first 10 days of
ker test influenced patient management in 84% of cases the menstrual cycle (i.e., follicular phase).80 A pregnancy
and was accurate in diagnosing both obstructive and non- test should be performed on the day of the procedure,
obstructive uropathy in 77% of cases. because pregnancy is one of the only absolute con-
Complications are, for the most part, related to percu- traindications to the procedure. Prophylactic antibiotics
taneous access to the upper collecting system and include (e.g., 100 mg of doxycycline, given twice daily) should be
pain, bleeding (retroperitoneal, parenchymal, or subcap- started on the day before the procedure and continued
sular hematoma), infection, sepsis, and damage or perfo- for 4 days afterward. The procedure is performed with
ration of the collecting system with resultant urinoma. It sterile technique after standard scrubbing and draping of
is possible to rupture the collecting system during fluid the perineum. IV conscious sedation usually is sufficient
infusion, making it important to limit perfusion pressures for patient comfort; paracervical anesthesia usually is not
to approximately 30 cm H2O. required.
A guiding catheter is inserted through the cervix
under direct visualization. Commonly used catheters
HYSTEROSALPINGOGRAPHY AND have an intrauterine retention balloon or a vacuum cup
FALLOPIAN TUBE RECANALIZATION that is placed on the cervix. These devices provide a
sterile conduit through which catheters and guidewires
Of all causes of infertility, up to 45% have been attributed may be introduced. Conventional HSG should be per-
to the female partner. Between 10% and 35% of female formed with diluted water-soluble contrast to confirm
infertility is due to tubal disease.76,77 The leading cause of proximal tubal occlusion and to localize the uterine
tubal disease is pelvic inflammatory disease (PID). Selec- cornua without obscuring the catheters. If HSG shows
tive salpingography and fallopian tube recanalization can flow through the fallopian tubes, no further steps are
be used to treat proximal tubal occlusion and has been taken (Fig. 23-23).
endorsed by the American Society for Reproductive Med- If the proximal tube is occluded, a 5-Fr catheter is
icine as primary treatment of tubal occlusion when one or advanced coaxially through the guiding catheter and
both tubes fail to fill at hysterosalpingography (HSG).76,78 used to selectively catheterize the tubal ostium. Full-
The proximal aspect (first 2 cm) of the fallopian tube is strength contrast is then injected. If proximal tubal ob-
most amenable to recanalization. Recanalization of the struction persists, efforts to clear the obstruction should
more distal fallopian tube is more technically challenging be made (Fig. 23-24). A coaxial microcatheter system with
706 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
FIGURE 23-23 Normal hysterosalpingogram. A, Initial image from normal hysterosalpingogram shows balloon retention catheter (straight
arrow) and flow through both fallopian tubes (curved arrows), consistent with patent bilateral tubes. B, Later image shows further distension of
the uterine cavity and contrast collecting in the peritoneum.
A B
C D
FIGURE 23-24 Fallopian tube recanalization. A, Hysterosalpingogram shows a left fallopian tube with intraperitoneal contrast spillage
but no filling of the right tube. B, Selective right salpingography confirms occlusion of the right fallopian tube. C, A microcatheter and wire
were manipulated across the occlusion. D, After removal of the microcatheter, repeat selective salpingography revealed patency of the right
fallopian tube.
a 3-Fr catheter and a 0.018-inch or smaller guidewire is on the other side, if necessary. A final HSG is obtained to
advanced through the 5-Fr outer catheter. When the mi- confirm and document tubal patency.
crocatheter has been advanced beyond the obstruction, A 0.035-inch hydrophilic guidewire placed directly
the guidewire is removed, and contrast is injected to through the 5-Fr catheter may cross the obstruction
check distal tubal patency. The microcatheter is then re- more easily and eliminate the need for microcatheters.81
moved, and contrast is injected through the 5-Fr catheter After successful guidewire traversal, the wire is re-
to evaluate the tube. Recanalization is then performed moved, and distal tubal patency is confirmed by ostial
23. UROLOGIC AND GENITAL SYSTEMS 707
injection through the 5-Fr catheter. The patient is observed or both fallopian tubes.80 Repeat recanalization is pos-
for 30 to 60 minutes after the procedure and advised that sible, and pregnancies have resulted after the second or
vaginal spotting may occur for 3 days or less. even third procedure.
Instead of using a guide sheath or balloon catheter, a Mild uterine cramping and vaginal bleeding are
5-Fr angle-tipped catheter can be advanced through the common after fallopian tube catheterization and should
cervix with direct visual guidance. HSG can then be per- resolve within 2 to 3 days. Low-grade fevers may develop
formed through the catheter. If the fallopian tube is ob- but infection is rare, especially with the use of prophy-
structed, the catheter can be used to select the ostium and lactic antibiotics. Tubal perforations occur in 2% to 5%
contrast injection performed. Ostial injection of contrast of patients and usually require no additional treat-
alone may clear the obstruction and result in fallopian ment.80 The radiation dose to the ovaries is generally
tube visualization. However, if the tube does not fill fol- less than 1 rad (10 mGy).87
lowing ostial injection, a glidewire or equivalent is ad-
vanced across the occluded segment. If the tube remains
occluded, either a glidewire or microcatheter and wire STERILIZATION BY FALLOPIAN TUBE
can be used to attempt traversal of the tube. Once the oc- OCCLUSION
cluded segment has been traversed, contrast injection
should be performed to further delineate the fallopian Permanent sterilization has been used as a means of
tube anatomy.82 At this point the tube may be patent and contraception for many years. Historically, sterilization
show only minimal persistent irregularity, which would has been performed surgically, with either open or lapa-
be interpreted as successful recanalization. If the tube roscopic tubal ligation or vasectomy. Approximately
remains occluded proximally, opens proximally but re- 700,000 tubal ligations are performed each year in the
mains occluded distally, or looks markedly irregular, the United States and roughly half of them are performed
patient will require other solutions (e.g., surgical tube separately from delivery (either vaginal or cesarean).88
repair, in vitro fertilization).83 Transcervical approaches to sterilization have been de-
veloped as a minimally invasive alternative to surgical
sterilization.88,89
Results and Complications
Reporting standards for selective salpingography and
Devices
fallopian tube recanalization have not been established,
which makes comparison of techniques, success rates, Two hysteroscopic sterilization methods are currently
and treatment strategies difficult.76 No convincing evi- available in the United States and approved by the FDA.
dence indicates that any one technique is superior. The Essure Permanent Birth Control Systems (Conceptus,
Technical success is high, with studies showing up to Inc.) method involves transcervical placement of a nickel
73% success opening at least one fallopian tube.76,84 titanium coil in the proximal fallopian tube. It measures
Multiple studies have shown fertility rates as high as 2 mm in diameter and is 4 cm long. It expands to fill the
20% to 34% following HSG and fallopian tube recanali- fallopian tube and induces an inflammatory response
zation (in selected patients though to have tubal disease that over several weeks creates fibrosis and eventual scar.
and occlusion per HSG).76,84-86 Because the device relies on fibrosis and scar formation, it
The rate of ectopic pregnancy is about 3% to 4%, which cannot be relied on for contraception immediately after
is comparable to the rate in the general population.80,83 placement. A hysterosalpingogram is repeated 3 months
Fallopian tubes that require only minimal manipulation after coil placement to confirm occlusion. Once bilateral
to reestablish patency are more likely to be associated occlusion is confirmed, the patient can discontinue other
with subsequent pregnancy than tubes requiring exces- means of contraception.
sive guidewire and catheter manipulation. Some patients The Adiana Permanent Contraception device (Hologic,
in the former category may have mucous plugs (which Inc.) was introduced in 2002. In contrast to the Essure
are flushed out by the initial selective contrast injection) device, the Adiana system combines a low energy radio-
without underlying mural disease. Although tubal dis- frequency ablation with deposition of a polymer matrix
ease does not preclude successful pregnancy, the preg- in the proximal fallopian tube. It is designed to be per-
nancy rates are higher when the tubes appear normal formed with hysteroscopic guidance.
at salpingography. In one series, 95% of patients with
tubal obstruction but normal tubes were successfully re-
Patient Selection
canalized, and 45% became pregnant.80
If pregnancy has not occurred within 6 months of Preprocedural evaluation should include a recent nor-
successful tubal recanalization, approximately 50% of mal Pap smear, negative chlamydia and gonorrhea cul-
evaluated patients are found to have reblockage of one tures, and negative pregnancy test. Contraindications to
708 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
transcervical fallopian tube occlusion are the desire to rates in the first year of follow-up, there was a 1.07%
maintain fertility, recent or current PID, prior tubal liga- failure rate.91,92
tion, immunosuppression, nickel allergy, unexplained
menometrorrhagia, pregnancy, and recent ("6 weeks)
delivery or termination of pregnancy.88,89 NONVASCULAR RENAL TRANSPLANT
COMPLICATIONS
Technique Approximately 18,000 kidney transplants were per-
The device can be placed with only moderate seda- formed in the United States in 2009, as recorded by
tion and both fallopian tubes can be occluded in the UNOS (United Network for Organ Sharing).93 The
same setting. Ideally the procedure is performed in most common nonvascular complications of kidney
the first 7 to 14 days following the patients menstrual transplantation are perinephric fluid collections, ob-
cycle (follicular phase). The patient is placed in a li- struction, and ureteral stricture. Many perinephric
thotomy position on the angiography table and the fluid collections are asymptomatic and sometimes
vulva and perineum are prepared and draped in a self-limited. Fluid collections associated with renal
standard sterile fashion.88 A sterile speculum is placed transplants include lymphoceles, urinomas, hemato-
and the cervix is visualized, then prepped. Typically, mas, seromas, and abscess. Ultrasound, CT, and MRI
a 12-Fr balloon catheter is placed and inflated to are used to detect and sometimes characterize these
minimize contrast leakage from the cervix. A hys- lesions.94 However, aspiration and drainage are typi-
terosalpingogram is then performed. The fallopian cally required for definitive diagnosis and treatment
tubes must be well visualized in order to proceed and and percutaneous drainage for diagnosis and treat-
visualization may require selective catheterization. ment is preferred over surgery in most patients.
Only if both tubes can be safely occluded should All of these fluid collections can cause symptoms
placement be performed, leading to the recommen- either from infection or mass effect. The most likely
dation that the most difficult-appearing fallopian structures to be compressed are the ureter and the iliac
tube be addressed first.88 The device has a 4.3-Fr vein. However, compression of the transplant renal vein,
outer diameter and once the fallopian tube is cannu- iliac artery and other pelvic veins has been reported.
lated, the device is advanced until the third of four Ureteral compression can be associated with obstruc-
radiopaque markers is at the level of the tubal ostium. tion, and hydronephrosis and iliac vein compression
The coil is deployed and the process is repeated on can be associated with deep vein thrombosis and pul-
the contralateral side. monary embolism.95,96
Results Urinoma
Successful placement of the Essure device has been Urinomas usually occur within the first several weeks of
reported in multiple studies to be 92% to 99%.88,90 transplant and are associated with a urine leak. Urine leak
The Essure device has been evaluated in the Essure following renal transplant is seen in up to 3% of cases
phase II and pivotal trials.88 Device placement was at- with mean onset of 45 days.97 Urine leaks are most com-
tempted in 745 patients between the two trials. Successful mon at the ureterobladder insertion and generally results
bilateral placement was performed in 88% of the phase from ureteral ischemia.97 Diagnosis is typically made with
2 trial and 90% of the pivotal trial. Ninety-seven percent a combination of imaging and aspiration or drain place-
of women who had successful bilateral coil placement ment. Aspirated fluid should be sent for analysis and will
were able to rely on the device for primary birth control, show a high creatinine level. Ultrasound of urinomas
and the device is effective in preventing pregnancy in typically shows an anechoic fluid collection with a pau-
99.8% of cases. As of 2005, more than 50,000 Essure devices city of septations and debris. The urine leak should be
have been placed worldwide, most with hysteroscopic identified with either antegrade nephrostogram or retro-
guidance.91 Currently, device placement with fluoroscopic grade nephrostogram/cystogram. Treatment should ad-
guidance is off-label. dress the urine leak with ureteral stent placement, either
A total of 770 women were enrolled in a trial using from above via PCN or from below with double-J ureteral
the Adiana system; 645 patients were actually treated. 92 stent. A double-J ureteral stent is preferred for long-term
Bilateral placement was achieved in 95% of patients. stent placement due to the decreased incidence of infec-
Evaluation with HSG was performed at 3 months to tion in the immunocompromised transplant patient.96
confirm tubal occlusion. Of the 645 women in the ini- The urinoma often resolves once the leak has been ad-
tial treatment group, 88% were able to rely on FTO dressed but if it persists or causes mass effect, a small-
for primary contraception, and based on pregnancy bore percutaneous drain is indicated.
23. UROLOGIC AND GENITAL SYSTEMS 709
A B
C D
FIGURE 23-25 Renal transplant hydronephrosis due to extrinsic compression by a lymphocele. A, Initial ultrasound scan shows a large
fluid collection superficial to the hydronephrotic transplant kidney. B, After percutaneous drainage and alcohol sclerosis of the lymphocele,
ultrasound shows that hydronephrosis has resolved. C, A 69-year-old woman 6 weeks after a renal transplant complained of urinary frequency
and had mildly elevated creatinine level. Initial ultrasound scan shows a large fluid collection (arrow) superficial to the hydronephrotic trans-
plant kidney that after drainage was revealed to be a lymphocele. D, The lymphocele also compresses the bladder (curved arrow). Percutaneous
drain was placed for decompression (arrowhead).
710 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
t-PA administration will likely need to be repeated several upper or middle polar calyx should be selected to facilitate
times per day with regular flushing of the catheter to ureteral catheterization. Internalized stents are preferred
maximize percutaneous drainage. over catheters that protrude externally to minimize the
risk of infection in this immunocompromised group of
patients. An antegrade nephrostogram is then done to
Ureteral Obstruction evaluate the collecting system and ureter. The PCN access
Ureteral obstruction in a transplant kidney may be diffi- can also be used to traverse a ureteral stenosis or occlusion
cult to distinguish from other causes of renal transplant and dilate the stenotic lesion. Ureteral stents can also be
dysfunction. Obstruction can result from multiple differ- placed from an antegrade access (Fig. 23-28).
ent etiologies, including blood clots, external compres- Ureteral strictures are treated successfully with balloon
sion, kinking, or frank anastomotic stricture (Figs. 23-26 dilation in about 60% to 70% of cases103,104 (Fig. 23-29).
and 23-27). Initial evaluation is done with ultrasound. However, the success of balloon dilation decreases with
Because the risk of PCN is low and the consequence of more chronic strictures and with longer stenoses.96,103,104
a delayed diagnosis of obstruction may be loss of the In renal transplants with ureteral leakage, percutaneous
transplant, a low threshold for PCN as a diagnostic chal- treatment with nephroureteral stents is successful in 59%
lenge is advocated.103,104 of cases.104 However, surgical repair of post transplant
The transplant ureter is prone to ischemic injury and urine leaks, especially in the early post transplant period,
stenosis in part because of the disrupted blood flow dur- is still considered the gold standard of therapy.
ing kidney harvest and transplant. The most common
sites of stenosis are the distal ureter and the ureterovesical
anastomosis. Extrinsic compression on the collecting sys-
tem by hematoma, lymphocele, or urinoma can also pro-
duce an obstruction. If obstruction coexists with a fluid
collection, percutaneous drainage of the fluid may relieve
the collection and the obstruction (see Fig. 23-25).
When planning PCN of a kidney transplant, it is impor-
tant to avoid entry into the peritoneum by making the
needle entry lateral to the transplant and skin incision.
Ultrasound is ideal for imaging guidance. An anterolateral
A
B
FIGURE 23-27 Outflow obstruction in a transplant kidney.
A, Typical ultrasound image of left pelvic transplant kidney with
FIGURE 23-26 Transplant kidney 2 days after transplant moderate hydronephrosis. B, Antegrade nephrostogram performed
with minimal urine output and small blood clots passing in urine. after percutaneous nephrostomy tube placement shows a low ure-
Antegrade nephrostomy catheter placed and antegrade teral obstruction at the ureterovesicular junction. There is also a mild
nephrostogram performed, showing the entire renal collecting stenosis in the midureter, likely representing a kink related to redun-
system filled with blood clot. dancy of the ureter.
23. UROLOGIC AND GENITAL SYSTEMS 711
C D
A B
712 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
Significant complications are very unusual.109,110,116 For many years, the standard therapy for TOA was
Mild flank pain and occasionally microscopic hematuria broad-spectrum IV antibiotics and surgical drainage with
occur.110,116 Low grade fevers are usually self-limited.116 washout when necessary. Percutaneous drainage is now
Sclerosis of parapelvic cysts carries the additional theo- the widely accepted first-line treatment when antimicro-
retical risk of damage to the adjacent hilar structures. bial agents alone are not effective.123 The only major (rela-
Pelvic-ureteric obstruction caused by sclerosis-induced tive) contraindications to this method are pregnancy and
fibrosis has been reported.118 pelvic neoplasm.
Surgical alternatives to percutaneous cyst aspiration Catheters may be placed by a transabdominal, trans-
and sclerosis include open surgical cyst unroofing, lapa- gluteal, or transvaginal route.121,123 When a transgluteal
roscopic cyst unroofing, and marsupialization of the access is chosen, entry close to the sacrum and inferior
cyst.111 However, these techniques are much more ex- to the pyriformis muscle is advisable to avoid major
pensive and usually involve general anesthesia. Most blood vessels and nerves.124,125 Also, pericatheter pain is
believe that surgical results are similar to percutaneous diminished when the tube runs below the pyriformis
sclerotherapy; however, direct comparisons are very dif- muscle. In one recent study of women with TOA, clinical
ficult due to the significant variations in technique. response rates for drainage and antibiotics versus antibi-
otics alone were 100% and 58%, respectively.126 All but
one of the 19 patients in the latter group later responded
TUBO-OVARIAN ABSCESS to percutaneous drainage. Additionally, patients in the
primary drainage group had shorter hospital stays and
In the United States, PID occurs in about 800,000 women had faster resolution of fever. Dewitt and associates121
per year, most of whom are younger than 25 years of age.119 noted that TOA greater than 8 cm in size were more
About one third of women hospitalized for PID develop a likely to require percutaneous drainage. Based on expe-
frank pelvic abscess. In premenopausal women, tubo- rience in 58 patients, Goharkhay and colleagues126 sug-
ovarian abscess (TOA) is commonly associated with PID. gested a threshold of #150 mL for primary drainage
In post-menopausal women, TOA is more often the conse- rather than a trial of medical management.
quence of underlying malignancy or diverticulitis.120 While
mortality has improved markedly over the past several de-
cades, morbidity remains high. Complications associated RENAL ABSCESS
with TOA include ectopic pregnancy, infertility, thrombo-
phlebitis, venous thrombosis, and chronic pelvic pain.121 Renal and perirenal abscesses usually result from ascend-
Ultrasound is the ideal imaging modality for TOA ing infection (simple urinary tract infection or pyelone-
diagnosis. Typical findings are thin-walled cystic pelvic phritis) or hematogenous spread. Risk factors for renal
masses with relatively uniform echogenicity in or adja- abscess include immunocompromised state, diabetes,
cent to the ovaries. Air-fluid levels and septations are underlying urinary tract abnormality (e.g., stone, dupli-
common. CT typically shows unilateral, multilocular, cated collecting system, vesicoureteral reflux, neurogenic
low-attenuation collections in the pelvis with thick, bladder, polycystic kidney disease), or an obstructive
enhancing walls122 (Fig. 23-30). mass (e.g., tumor, cyst, lymphocele, urinoma).127 The
A B
FIGURE 23-30 Tubo-ovarian abscess (TOA). A, Ultrasound shows a fluid collection adjacent to the right ovary consistent with TOA. The
patient had a fever, elevated white cell count, pelvic pain, and a palpable pelvic mass on bimanual examination. B, Image following computed
tomographyguided drain placement shows transabdominal percutaneous drain into the abscess. Purulent material (20 mL) was aspirated.
Left pelvic collection was also drained percutaneously.
714 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
76. Thurmond AS. Pregnancies after selective salpingography and 101. Hedegard W, Saad Wael EA, Davies M. Management of vascular
tubal recanalization. Radiology 1994;190:11. and nonvascular complications after renal transplantation. Tech
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78. Guidelines for practice. Birmingham, Ala: American Fertility Society; 103. Benoit G, Alexandre L, Moukarzel M, et al. Percutaneous ante-
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79. Thurmond A. Selective salpingography and fallopian tube recanali- 1993;150:34.
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C H A P T E R
24
Interventional Oncology
Eric J. Hohenwalter, David Sella, William Rilling
The number of patients diagnosed with cancer each year in the United States and around the world. Other less
is growing. In 2002, there were 10.9 million new cases common primary liver cancers include cholangiocar-
worldwide, 6.7 million deaths, and 24.6 million people cinoma, fibrolamellar carcinoma, hepatoblastoma, and
alive with cancer (within 3 years of diagnosis).1 The most angiosarcoma of the liver.
commonly diagnosed cancers are lung, breast, and
colorectal, and the most common causes of cancer death Etiology and Natural History
are lung, stomach, and liver cancer.2 Primary liver cancer Hepatitis B virus (HBV) and hepatitis C virus (HCV)
is the sixth most common cancer worldwide and the infections are the main risk factors for HCC.5 Risk fac-
incidence of primary liver cancer is increasing. However, tors for viral hepatitis include contaminated blood trans-
metastatic tumors to the liver are more common than fusions, intravenous drug use, needle sharing, and unsafe
primary tumors.3 Significant improvements in chemo- sexual practice. HCC develops from HBV and HCV after
therapy and surgical options as well as the advancement a latency period of one to three decades.6 Other risk
of endovascular and image-guided treatments and the factors for developing HCC include alcohol abuse, hemo-
expanded role of interventional oncology have led to in- chromatosis, aflatoxin exposure, diabetes mellitus, and
creased survival in these patients. nonalcoholic fatty liver disease. Studies have demon-
Several factors are important when determining the strated a dose-response relationship between alcohol
most effective therapy for a patient diagnosed with can- consumption and the risk for HCC development.7 As
cer. Previous treatment, extent of disease, and perfor- with alcohol, most risk factors are linked to HCC through
mance status are just a few of the important factors to the development of cirrhosis. However, up to one fourth
consider when evaluating patients in clinic. In addition, of HCC cases arise in nonfibrotic livers.8 If untreated, the
the goals of therapy may vary widely from patient to 1-, 2-, and 3-year survival rates in patients with HCC is
patient, from curative, to tumor downstaging for surgery 54%, 40%, and 28%, respectively.9
or transplantation, to palliative therapy. As with most
solid organ tumors, the consideration of which patients Clinical Features
will benefit from the available treatment options should Patients with HCC often have symptoms related to their
be made by the careful assessment of a multidisciplinary underlying liver disease as well as their malignancy. The
team of physicians. prognosis of solid tumors is generally related to tumor
stage at presentation and thus tumor stage ultimately
guides treatment decisions. However, assessment of
LIVER clinical outcome is particularly complex in HCC because
the underlying liver function also affects prognosis. His-
Hepatocellular Carcinoma and Other torically, HCC was classified by the traditional TMN
Primary Liver Tumors (Online Cases 25, staging system based on pathologic findings without
consideration of underlying liver function.10 The Okuda
58, 79, and 101)
Staging System takes tumor size and liver function
There were an estimated 17,550 new cases and 15,420 into account; however it is unable to adequately stratify
deaths due to primary liver cancer in 2005 in the patients with early or intermediate stage disease11
United States. These numbers yield an incidence of (Table 24-1). The Child-Pugh and the Model for End-stage
5.4 per 100,000.4 Hepatocellular carcinoma (HCC) ac- Liver Disease (MELD) assessment classifications only
counts for the vast majority of primary liver cancer consider liver function. The Barcelona Clinic Liver Cancer
718
24. INTERVENTIONAL ONCOLOGY 719
TABLE 24-1 Okuda Staging System size of the lesion. Some form of imaging is required to
evaluate the extent of disease.
SCORE
Criteria 0 1 ULTRASOUND
Tumor size "50% of liver #50% of liver Ultrasound is an excellent and inexpensive screening tool
Ascites Absent Present for HCC diagnosis, but it is highly dependent on the
Albumin (g/dL) $3.0 "3.0 operator. HCC usually appears as a round or oval mass
Bilirubin (mg/dL) "3.0 #3.0 with sharp boundaries. HCC may exhibit a hypoechoic,
Stage I, score 0; stage II, score 1 or 2; stage III, score 3 or 4. isoechoic, or hyperechoic appearance with respect to
the surrounding liver parenchyma. A small hyperechoic
HCC may be indistinguishable from hemangioma.15
(BCLC) staging system is based on the combination of The reported sensitivity of conventional ultrasound in
data from several independent studies representing dif- the detection of HCC ranges from 35% to 84%.16 Using
ferent disease stages and treatment strategies.12-14 This Doppler or power Doppler sonography to evaluate for
classification scheme comprises four stages that match hypervascularity or portal venous invasion can increase
the best candidates for the best therapies and includes the accuracy in the detection of HCC; however, detection
variables related to tumor stage, liver functional status, of smaller lesions (!1 cm) remains problematic.
physical status, and cancer-related symptoms (Fig. 24-1).
COMPUTED TOMOGRAPHY
Imaging Computed tomography (CT) is a common imaging mo-
The tests used to diagnose and stage HCC include imag- dality used for detection and diagnosis of HCC. A three-
ing, alpha-fetoprotein (AFP) serology, and biopsy. Opti- phase technique including noncontrast, early arterial, and
mal imaging depends on the clinical scenario and the portal venous (PV) inflow imaging is standard of care.17
HCC
The value of adding delayed scans (e.g., 3 to 5 minutes after MAGNETIC RESONANCE IMAGING
contrast injection) to depict pathologic tumor washout has As with CT, hypervascularity with delayed washout in
been demonstrated.18 HCC typically appears as a hyper- a cirrhotic liver are characteristics most consistent with
vascular lesion in the early arterial phase with washout to HCC (Fig. 24-3). As with CT and ultrasound, the detec-
an isodense or hypodense appearance in the portovenous tion and characterization of lesions smaller than 1 cm
phase (Fig. 24-2). In addition to the number and size of le- remains problematic. However, with magnetic reso-
sions, patency of the portal vein and the presence of extra- nance imaging (MRI), the criteria for evaluation of focal
hepatic disease can be assessed. According to American lesions in cirrhotic liver can be expanded from vascular-
Association for the Study of Liver Disease (AASLD) and ity alone to cellular density and tissue composition by
European Association for the Study of the Liver (EASL) means of precontrast sequences and diffusion-weighted
guidelines, hypervascularity with washout in the PV phase MRI, to the presence of Kupffer cells by means of uptake
on two imaging examinations for small lesions (1 to 2 cm) of superparamagnetic particles of iron oxide and to the
or one imaging examination for larger lesions (#2 cm) is integrity of hepatocellular function and biliary excretion
diagnostic of HCC. A biopsy is not necessary in these cases. by means of hepatobiliary contrast agents.20 Whereas the
However, for small lesions ("1 cm), it is difficult to distin- use of these agents is not standard practice, they may
guish between regenerative nodules and HCC. In addition, prove to increase the sensitivity and specificity of lesion
arteriovenous shunts may mimic small HCCs.19 detection and diagnosis of HCC with MRI, especially in
A B
FIGURE 24-2 Hepatocellular carcinoma. Computed tomography scan demonstrating a hypervascular tumor in the early arterial phase
(A) with subsequent washout on delayed imaging (B).
A B
FIGURE 24-3 Hepatocellular carcinoma. Magnetic resonance imaging demonstrating hypervascular tumors in the early arterial phase
(A) with subsequent washout on delayed imaging (B).
24. INTERVENTIONAL ONCOLOGY 721
the case of lesions that are less than 1 cm in size. Burrel the liver that is going to be removed, inducing hypertrophy
and colleagues reported a sensitivity of 100% for lesions in the portion of the liver that will be left behind,
larger than 2 cm, 89% for lesions between 1 and 2 cm, known as the liver remnant, over a period of 3 to
and 34% for lesions smaller than 1 cm.21 4 weeks (Fig. 24-4). This technique increases the ability
to resect the liver safely.28
Treatment Transplantation represents effective treatment for
For patients diagnosed with HCC, there are many the underlying liver disease as well as the cancer. How-
treatment options available that will potentially have ever, the surgical risks of graft failure and infection, the
a positive impact on survival.22 To achieve the best shortage of donor organs leading to a long waiting list,
outcome requires careful selection of candidates for and the risks associated with lifelong immunosuppres-
each treatment option. Because this is a complicated sion therapy can be seen as disadvantages.29 The most
disease process and there are multiple potentially widely accepted Milan criteria include patients with a
beneficial therapies, patients with HCC should be solitary tumor of 5 cm or less in diameter or patients
referred to a multidisciplinary team of doctors, in- with no more than three tumors, each 3 cm or less in
cluding hepatologists, oncologic surgeons, transplant diameter, and no invasion of major blood vessels,
surgeons, interventional radiologists, and medical lymph nodes, or extrahepatic sites.30 Using these crite-
oncologists, among others. ria, 4-year survival rates of up to 85% have been re-
ported. Slightly expanded thresholds such as the UCSF
MEDICAL THERAPY criteria (single lesion !6.5 cm or two lesions !4.5 cm
Historically, no systemic chemotherapy has improved with total tumor diameter !8 cm) have also shown fa-
survival in patients with advanced HCC.23,24 However, vorable 1-and 5-year survival rates of 92.1% and 80.7%,
sorafenib (Nexavar) is an oral tyrosine kinase inhibitor respectively.
agent that has shown some survival benefit in patients
with advanced HCC. Sorafenib inhibits tumor cell pro- PERCUTANEOUS THERAPY
liferation and angiogenesis. In a recent multicenter, TRANSCATHETER ARTERIAL CHEMOEMBOLIZATION
phase III clinical trial with more than 600 patients, me- AND BLAND EMBOLIZATION Liver tumors, both
dian survival in patients treated with sorafenib was primary and metastatic, receive their blood supply
nearly 3 months longer than those treated with pla- predominantly from the hepatic artery.31 Because the
cebo.25 The most common side effects of sorafenib in the normal liver has dual blood supply (75% portal vein,
trial were diarrhea, weight loss, hand-foot skin reac- 25% hepatic artery), chemoembolization delivers local-
tions, and alopecia. ized treatment to tumors without significant damage to
the adjacent parenchyma. Chemoembolization also de-
SURGICAL THERAPY livers higher doses of chemotherapeutic agents to liver
For treatment with curative intent, surgical resection tumors than does systemic therapy. In addition, the em-
(partial hepatectomy or liver transplantation) has been bolization component of chemoembolization prolongs
at the forefront of treatment options for patients with the dwell time of the chemotherapeutic agents within
HCC (see Fig. 24-1). However, HCC often occurs in pa- the liver, thereby limiting systemic toxicity.32 Regarding
tients with cirrhosis, which increases the risks associ- transcatheter arterial chemoembolization (TACE), varia-
ated with operation. Advances in perioperative care, tions in protocol exist, including the chemotherapeutic
patient selection, and radiologic assessment have led to used, use of lipiodol, and the type of embolic agent used
decreased morbidity and mortality associated with sur- to decrease blood flow. In the United States, doxorubi-
gical resection.26 Some of the most important factors in cin, cisplatin, and mitomycin are the drugs most often
determining whether surgery is an option for patients used.33 Our protocol for a standard chemoembolization
with HCC include performance status, hepatic function is 50 mg doxorubicin, 10 mg mitomycin, and 100 mg
and reserve, extent and location of tumor, and the pres- cisplatin. Lipiodol is an iodized ester from poppyseed
ence of vascular invasion. Some of the surgical options oil. When it is injected into the hepatic artery, it is cleared
include tumor excision, trisegmentectomy, and right or from normal hepatic tissue but accumulates in tumor
left hepatectomy. cells because of the absence of Kupffer cells.34
To improve results following hepatectomy, portal vein Patient Selection Several factors are important
embolization may be necessary. In cirrhotic patients in when determining whether a nonoperable patient is an
whom resections to remove more than two functional seg- appropriate candidate for chemoembolization. In pa-
ments are planned, portal vein embolization should be tients with advanced liver disease, treatment-induced
considered as a preoperative adjunct to induce hypertro- liver failure may offset the antitumoral effect or sur-
phy of the liver remnant.27 Portal vein embolization is a vival benefit of the intervention.35 Therefore some of the
technique used to occlude portal inflow to the portion of predictors of outcome are related to neoplastic burden:
722 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
C D
E F
FIGURE 24-4 Portal vein embolization before right trisegmentectomy. A, Access is gained to a right portal vein branch with sonographic
guidance. B, A vascular sheath has been placed, followed by portography, which shows distortion of right portal branches by tumor. C, Portal
branches to segment IV have been embolized (arrow). D and E, Right portal venous branches are engaged and then occluded. F, Final porto-
gram shows complete obstruction of branches to liver segments IV-VIII.
24. INTERVENTIONAL ONCOLOGY 723
tumor size, number of tumors or percentage of liver Absolute contraindications for chemoembolization
involved with tumor, and extent of vascular invasion, if include intractable systemic infection and extensive
present. The degree of liver dysfunction should also be extrahepatic disease. Relative contraindications include
evaluated. This can be accomplished with the MELD portal vein invasion, the presence of encephalopathy,
assessment. Exclusion criteria base on specific labora- and unrelieved biliary obstruction. Several studies have
tory values have not been definitively established. In demonstrated the safety and effectiveness of TACE
addition, the performance status of the patient is vital in in patients with portal venous invasion when chemoem-
determining whether a patient will be able to tolerate bolization is performed in a subselective manner.37,38
chemoembolization as a treatment for the liver tumor. Other relative contraindications include uncorrectable
Two scales of performance status include the Karnofsky coagulopathy, significant arteriovenous shunting, and
index and the Eastern Cooperative Oncology Group significant renal insufficiency. These are relative contra-
(ECOG) toxicity and response criteria (Tables 24-2 and indications because these may be correctable or the
24-3). The best candidates are patients with liver domi- treatment regimen may be altered to accommodate the
nant disease (no significant extrahepatic disease), pre- abnormality. For example, in the case of a patient with
served liver function, and a performance status of angiographically visible shunting within the tumor, a
ECOG 0 or 1. bland embolization could be performed before chemo-
In addition to prolonging survival and/or treating embolization in order to reduce the shunt and ensure
symptoms in unresectable patients, locoregional thera- adequate treatment of the tumor.
pies have been shown to maintain patients on the trans- Technique Patients receive preprocedure hydra-
plant waiting list as well as downstage the disease in tion as well as antiemetics and steroids (Box 24-1).
some patients.36 Preprocedure antibiotics are altered for the patient
who has a compromised sphincter of Oddi from prior
TABLE 24-2 Eastern Cooperative Oncology Group surgery or biliary stent placement. These individuals
Performance Status are at increased risk for infection and abscess forma-
tion following chemoembolization.39,40 For these pa-
Grade ECOG
tients, we prescribe moxifloxacin 400 mg daily for 10
0 Fully active, able to carry on all predisease performance days before the procedure. Diagnostic arteriography
without restriction
of the celiac and superior mesenteric arteries is essen-
1 Restricted in physically strenuous activity but
ambulatory and able to carry out work of a light or tial to identify the arterial supply to the tumor as well
sedentary nature (e.g., light house work, office work) as aberrant vessels supplying the tumor or extrahe-
2 Ambulatory and capable of all self-care but unable patic structures. The arteriogram should be carried out
to carry out any work activities. Up and about more to the venous phase to evaluate the patency of the por-
than 50% of waking hours
tal vein. A microcatheter is then used to selectively
3 Capable of only limited self-care, confined to bed
or chair more than 50% of waking hours catheterize the tumor arteries. It is also important to
4 Completely disabled. Cannot carry on any self-care. evaluate and identify any arteriovenous shunting,
Totally confined to bed or chair which has been reported to occur in 31% to 63% of
5 Dead cases between second order branches41 (Fig. 24-5).
A B
C D
FIGURE 24-5 Hepatocellular carcinoma. A and B, Celiac arteriogram demonstrating lesion within the right hepatic lobe. Notice the early
appearance of the portal vein (arrow). C and D, Subselective arteriogram demonstrating arterial portal shunting within the tumor.
24. INTERVENTIONAL ONCOLOGY 725
Practice patterns vary as to whether a superselective, patients treated with chemoembolization with those given
segmental, or lobar approach is performed (Fig. 24-6). supportive care and demonstrated improved survival at 1,
However, treatment of the entire liver in one session is 2, and 3 years. Another study by Llovet and colleagues
associated with increased mortality.42 It may be neces- compared chemoembolization and hepatic arterial embo-
sary to evaluate extrahepatic arterial supply to the tu- lization with supportive care and demonstrated a survival
mor as well, such as the inferior phrenic artery. In a ret- benefit in the embolization treatment groups.45
rospective study of more than 2300 procedures, TACE Complications Postembolization syndrome is char-
through an extrahepatic collateral was considered in acterized by abdominal pain, fever, anorexia, nausea,
25% of cases43 (Fig. 24-7). A variety of TACE protocols and fatigue. The cause is not completely understood
exist and there is great variability in the amount and but several theories exist including distention of
type of the chemotherapeutic agents used, type and the liver capsule, tumor necrosis, and ischemia of
amount of embolization agents, and sequencing of liver parenchyma.46 The severity of symptoms is vari-
embolization. able. They may last as long as 10 days and may occa-
Results Chemoembolization has been shown to be a sionally require an extended hospital admission. The
safe and effective treatment for selected patients with postembolization syndrome occurs in up to 90%
HCC. Two prospective, randomized trials demonstrating of patients following chemoembolization and for
the survival benefits of chemoembolization in HCC have that reason is considered a side effect rather than a
been published. A study by Lo and colleagues44 compared complication.47
C
FIGURE 24-6 Hepatocellular carcinoma. A, Contrast computed tomography scan in the arterial phase reveals a large hypervascular mass
in the right lobe of the liver with central puddling of contrast. B, Superior mesenteric arteriography with replaced right hepatic artery confirms
a large vascular mass with displacement of vessels. C, Following chemoembolization, flow has been abolished and lipiodol has accumulated
within the tumor.
726 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
Nontarget embolization, bile duct injury, and hepatic chemoembolization.48 In contrast to normal hepatic
failure are the potentially most severe complications parenchyma, intrahepatic bile ducts do not have dual
following chemoembolization (Table 24-4). Nontarget blood supply. Rather, they are fed exclusively from he-
embolization is defined as the inadvertent distribution patic arterial branches that give off a vascular plexus
of chemotherapeutic agents into unintended territories. around the bile ducts.49 Therefore, ischemic bile duct
Diagnostic arteriography prior to infusion of chemo- injury can occur following chemoembolization.
therapeutic agents is vital to identify any extrahepatic
arterial variants in the treatment region. Nontarget YTTRIUM-90 RADIOEMBOLIZATION Normal hepatic
embolization of a gastric artery or the gastroduodenal parenchyma is very sensitive to tumoricidal radiation
artery can cause gastrointestinal ischemia. If TACE doses. External beam radiation has had a limited role,
cannot be performed distal to the extrahepatic artery, in that as doses greater than 35 Gy have been shown to
embolization of the extrahepatic artery (with coils, if cause the development of radiation-induced liver dis-
safe) can be effective in preventing complications re- ease. Radioembolization is defined as the intraarterial
lated to nontarget embolization.31 Hepatic failure is delivery of radioisotope-labeled particles that become
more likely to occur in patients with impaired hepatic embedded in the tumor preferentially to surrounding
function prior to treatment. Acute liver failure has parenchyma because of differences in vascular supply.50
been reported in up to 2.3% of patients following Yttrium-90 (90Y) is a pure beta emitter and decays to 90Zr
24. INTERVENTIONAL ONCOLOGY 727
with a physical half-life of 64.2 hours. The energy has phase, patients undergo an angiogram to map the arte-
a mean tissue penetration of 2.5 mm and a maximum rial system and embolize any vessels that would allow
penetration of 11 mm. There are two commercially the microspheres to enter the gastrointestinal tract (i.e.,
available agents: SIR-Spheres (Sirtex Medical Ltd, Lane skeletonize the hepatic circulation).51 A superior mesen-
Cove, Australia) and TheraSphere (MDS Nordion, Ottawa, teric angiogram is performed to detect replaced or ac-
Canada). The 90Y is bound to either glass or resin micro- cessory hepatic arteries. In addition, the arteriogram is
spheres and delivered into the hepatic arteries via a carried out to the venous phase to evaluate the status of
microcatheter. To optimize safety and efficacy, radiation the portal vein. A celiac arteriogram and subsequent
dose planning and administration is modified on the selective hepatic angiography is performed to define
basis of tumor and liver volumes. Flow dynamics cause the hepatic and tumoral anatomy and to evaluate for
the particles to travel preferentially to the tumor. anatomic variants (Fig. 24-8). This step is critical in that
Patient Selection A Consensus Panel Report51 that the presence of unrecognized collateral vessels with
was published in 2007 provides detailed guidelines in consequent infusion of radioactive microspheres could
regard to patient selection for radioembolization. A lead to gastrointestinal ulceration, pancreatitis, and
summary of some general patient selection criteria and irradiation of other nontarget sites.54 For this reason,
contraindications are included in Box 24-2. Because a aggressive prophylactic embolization of these aberrant
small amount of adjacent liver will be affected by the vessels before therapy is essential. The gastroduodenal
radiation, sufficient hepatic reserve is required. Param- artery (GDA) is virtually always embolized to its origin
eters of adequate hepatic reserve include lack of ascites, with microcoils. Some of the relatively common ves-
normal synthetic liver function (e.g., albumin #3 g/dL) sels of interest include the right gastric, esophageal,
and normal total bilirubin ("2 mg/dL).52 Performance accessory left gastric, falciform accessory phrenic, and
status is also critical in patient selection and good can- supraduodenal or retroduodenal arteries. Once the
didates have a performance status of ECOG 0-2. An arterial anatomy has been evaluated and the aberrant
absolute contraindication to radioembolization is the gastrointestinal supply, if present, is embolized, the
predicted administration of a dose of at least 30 Gy to degree of lung shunting through the tumor must be
the lungs in a single treatment or greater than 50 Gy as estimated. To this end, 5 mCi of 99mTc-labeled macroag-
a cumulative dose on multiple treatments53 (see later gregated albumin particles is injected through the
discussion). microcatheter into the desired liver distribution. Single
Technique Starting a 90Y program is complicated. photon emission computed tomography gamma imag-
The treatment itself consists of two phases. In the first ing is done afterward to detect shunting of the albumin
728 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
C D
E
24. INTERVENTIONAL ONCOLOGY 729
particles into the pulmonary or gastrointestinal vascu- pneumonitis is a theoretical concern with 90Y treat-
lature. This information is then used to calculate an ment. Previous preclinical and clinical studies have
appropriate treatment dose.51 Specific dosimetry calcu- demonstrated that as much as 30 Gy to the lungs can be
lations have been described previously and are beyond tolerated with a single injection.54
the scope of this text.55
The second phase is the delivery of the microspheres. PERCUTANEOUS ABLATION Tissue ablation as a
Radiation safety is an important consideration in this form of treatment has gained increasing popularity over
procedure. 90Y is a beta emitter; therefore, the primary the past few decades. The development of improved
concern is exposure to the eyes, skin, and hands.51 If the devices and imaging modalities continue to push image-
delivery system becomes compromised, radioactive guided thermal ablation to the forefront of treatment in
contamination is a concern and steps should be taken to selected primary and secondary malignancies, medi-
prevent the spread of contamination. cally inoperable patients, and as palliative treatment.65
The 90Y infusion varies depending on the agent being Tissue ablation generally falls under one of two catego-
used, the location of the catheter, and the vessel undergo- ries: thermal ablation and chemical ablation. Thermal
ing infusion. The delivery is dependent on blood flow ablation includes technologies such as radiofrequency
through the hepatic artery distal to the catheter tip. Ra- ablation, microwave ablation, cryoablation, laser abla-
diation monitoring must be used to establish when opti- tion, and high-intensity focused ultrasound (HIFU).
mal delivery has been achieved. Typical surface radiation These techniques cause cell death by directly altering
dose rates from the patient will be less than 1 mrem/hr the temperature of the tumor. Chemical ablation in-
after implantation. Therefore, standard biohazard pre- volves infusing substances such as absolute ethanol into
cautions are sufficient to protect from exposure to others tumors, which directly produces necrosis.
after they have been discharged.51 Radiofrequency ablation (RFA) has the most substan-
Results Several studies have demonstrated the tial track record of the various thermal ablation tech-
therapeutic benefits of radioembolization for primary nologies used in HCC. The goal is to create a zone of
liver cancer in patients with advanced, unresectable coagulative necrosis of 0.5 to 1 cm around a lesion to
disease.56-59 Kooby and colleagues60 have compared ra- achieve a tumor-free margin.65 Tumor recurrence is
dioembolization to chemoembolization in a series of significantly reduced when a 1-cm tumor free margin is
retrospectively studied patients and concluded that ra- achieved with operative resection.66 RFA involves the
dioembolization and chemoembolization have similar insertion of percutaneous straight or expandable elec-
effectiveness and safety profiles. Time to progression trodes directly into a tumor (Fig. 24-9). Delivery of
and survival benefit in general varies by initial tumor high-frequency alternating current (200 to 1200 Hz)
stage and liver function. In addition, Kulik and associ- causes ionic agitation in the tissues, leading to fric-
ates61 concluded that radioembolization may have a tional heat. Local tissue temperatures are increased to
role in downstaging patients to fall within Milan crite- a targeted range of 60 to 100 C resulting in cellular
ria for liver transplantation. protein denaturation, cell membrane dysfunction, and
Complications As in chemoembolization, poste- coagulative necrosis.67 When temperatures greater
mbolization syndrome may develop following radio- than 100 C are reached, carbonization and charring
embolization treatment, although the symptoms are usually occur, with less effective energy transmission
usually less severe. Fatigue, nausea, vomiting, an- and diminished volume of the ablation zone.67 The ap-
orexia, fever, abdominal pain, and cachexia have been plied current in RFA exits the body through grounding
reported.62 Other potential complications include he- pads placed on the patient, generally at the thigh.
patic dysfunction, biliary injury, and gastrointestinal Treatment of lesions in close proximity to high-flow
complications resulting from nontarget embolization. vessels (#3 mm in diameter) requires consideration of
Altered hepatic function may predispose patients to the heat sink effect. Temperature variations are lim-
the hepatotoxic effects of radioembolzation.63 Kennedy ited by flowing blood, which carries the deposited
and colleagues64 observed radiation-induced liver dis- heat away, essentially increasing the chance of tumor
ease (elevated liver enzymes, anicteric hepatomegaly, progression. There are several commercially available
ascites) in 4% of patients after radioembolization with RFA devices, which use varied techniques to maximize
resin microspheres. The potential gastrointestinal com- the target ablation zone. Examples of a few RF devices
plications result from the inadvertent spread of micro- include the Valleylab RF Ablation Generator, Boston
spheres to the gastrointestinal tract, which results in Scientific LaVeen RF ablation system, and the Angio-
ulceration. As mentioned previously, meticulous map- dynamics RITA medical system.
ping, identification, and embolization of any potential Cryoablation also utilizes percutaneously placed
gastrointestinal arterial supply arising from the treat- probes. Room temperature argon gas travels from an
ment zone can prevent this untoward event. Radiation area of high pressure to the tip of the probe where it
730 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
A B
C D
FIGURE 24-9 Radiofrequency (RF) ablation for hepatocellular carcinoma. A, A pneumothorax has been induced to allow transthoracic
entry into the lesion in the dome of the liver. Ethiodol from prior chemoembolization demarcates the tumor. B, A second pass is required for
central needle placement. C, An RF probe is advanced to the far end of the lesion. D, The tines are deployed, and ablation is begun.
meets an area of low pressure and is allowed to rapidly When treating lesions near vessels larger than 3 mm in
expand within the sealed probe tip (a closed-loop, gas diameter, consider the cold-sink phenomenon, which
expansion system).68 The rapid expansion of the gas is analogous to the heat sink that interferes with RFA (see
causes a temperature decrease (Joule-Thompson effect), earlier discussion). Cryoablation generally entails stan-
which is transferred by conduction and convection to the dard protocols of multiple freezing stages with periods
probe tip, achieving a temperature of less than %40 C of interspersed active thawing. The currently available
within seconds. Temperatures of at least %20 to %40 C cryotherapy systems in the United States use compressed
are required to cause cell death and adequate tumor-free argon gas for cooling, which requires storage of large
margins, generally considered to be greater than 1 cm.69 pressurized containers. Advantages over RFA include the
Cryoablation causes direct and indirect cell death by in- ability to use multiple simultaneous probes, the ability to
tracellular and extracellular ice crystal formation and actively monitor the cryoablation zone with multiple im-
small vessel thrombosis.65 aging modalities, and decreased intraprocedural pain.70
24. INTERVENTIONAL ONCOLOGY 731
Microwave ablation involves the insertion of micro- survival and disease-free survival between the two
wave-transmitting antennae into a tumor. The micro- groups.78 There are fewer data regarding the safety
waves generate an oscillating electromagnetic field and efficacy of cryoablation and microwave ablation
with a frequency greater than 900 MHz.71 The weak for HCC.79 However, in retrospective analysis of
unequal dipoles of surrounding water molecules ori- 288 patients with HCC treated with percutaneous
ent with the field, the field oscillates, and the water microwave ablation, 1-, 2-, 3-, and 5- year survival
molecules oscillate rapidly, producing friction and rates were 93%, 82%, 72%, and 51%, respectively.80
heat.71 Advantages of microwave ablation over RFA Complications Knowledge of the potential compli-
include creation of a wider ablation zone with de- cations associated with percutaneous ablation is critical in
creased charring, increased temperatures within a assessing the risks of the procedure for each patient.
shorter time, less heat sink effect, and the ability to Proper patient selection and technique will help limit the
treat with multiple probes simultaneously. The abla- risk of procedural complications. An overall complication
tion system requires a microwave generator, power rate of 8.9% was observed in a meta-analysis of 82 inde-
distribution system (flexible coaxial cable), and micro- pendent reports with a total of 3670 patients.81 The most
wave antennae. No prospective trials have compared common complications included hemorrhage, abscess,
microwave and RFA ablations. and biliary stricture. Another potential complication is
Patient Selection and Technique The goal for any tumor lysis syndrome, which has been described after
ablative therapy should be to obtain complete destruc- both RFA and cryoablation of large tumor.82,83 This is an
tion of the tumor and some surrounding margin. Local uncommon systemic complication that may present with
ablation of tumors requires careful planning regardless severe thrombocytopenia and hepatic or renal failure.
of the method of destruction. The geometry produced Tumor lysis syndrome occurs more frequently with cryo-
by the ablation can be somewhat unpredictable and ablation than with the heat based methods, likely due to
neglecting to ensure complete coverage can lead to the mechanism of tissue destruction.65
treatment failure.72 Therefore, tumor size and location
are vital when treating patients with one of the ablative Colorectal Liver Metastases
therapies in order to choose the appropriate probe size
and number. Durable success of ablation and resultant Etiology and Natural History
improved survival depends on complete ablation of the Colorectal cancer (CRC) is the third most common can-
tumor.73 The likelihood of complete ablation decreases cer in the United States, with nearly 147,000 new cases
with increasing tumor size, and multiplicity of tumor and approximately 50,000 deaths reported annually.84
compounds this consideration.74 The liver is the major site of metastastic disease. Liver
Pretreatment imaging must accurately define the metastases from CRC are common and can be found in
location of each lesion with respect to surrounding up to 80% of patients diagnosed with CRC.85 Synchro-
structures. As mentioned earlier, treatment of a lesion nous hepatic metastases may be identified in 10% to 20%
that is close to a major vessel may result in suboptimal of patients with colorectal cancer.86 Without treatment,
results. In addition, ablation of lesions which are close survival for patients with CRC and liver metastases is
to portions of the gastrointestinal tract, diaphragm, less than 1% at 5 years.87
heart, and kidney may induce injury to the structure.
Likewise, central lesions treated with ablation may be Imaging
at increased risk for bile duct injuries. Various tech- Ultrasound, CT, and MRI are all commonly used in the
niques have been used to protect adjacent structures evaluation of hepatic metastases. The appearance can be
during ablation, including the use of hydrodissection quite variable, but in general, metastases appear similar
or the instillation of fluid (saline, D5W). 73 to the gross morphology of the primary tumor.88 Colorec-
Results There are substantial data supporting the tal cancer metastases usually appear as hypovascular
role of percutaneous RFA as an effective, safe, first- lesions on contrast-enhanced CT and MRI. Positron-
line therapy for cirrhotic patients with HCC smaller emission tomography (PET) and PET-CT also play a
than 3 cm who are not candidates for surgical resec- crucial role in the diagnosis and staging of patients with
tion or liver transplantation.75,76 In fact, recent studies colorectal metastases. Unlike HCC, there are no specific
have demonstrated 5-year survival rates ranging from imaging criteria for metastatic lesions that allow con-
51% to 76% in Childs A patients.77 These results have fident diagnosis. Therefore, pathologic confirmation is
raised the question as to whether RFA should be first- usually necessary.
line therapy for some patients with HCC smaller than
3 cm. A recent randomized controlled trial comparing Treatment
resection versus ablation in patients with Childs A Although liver metastases from CRC previously car-
cirrhosis and solitary HCC smaller than 5 cm failed ried a dismal prognosis, advances in systemic therapy,
to show statistically significant differences in overall interventional oncology, and surgical techniques have
732 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
improved survival in this disease. The appropriate mentioned previously, there are two commercially avail-
therapy and timing of treatment should be individu- able agents (SIR-Sphere and TheraSphere). Currently,
alized and determined by a multidisciplinary team of SIR-Sphere is FDA approved for patients with meta-
medical oncologists, radiation oncologists, interven- static CRC (Fig. 24-10). In a metaanalysis of 19 studies
tional radiologists, and surgeons. and 792 patients with metastatic CRC treated with ra-
dioembolization (SIR-Sphere and TheraSphere), response
MEDICAL THERAPY rates of approximately 80% and 90% (as first-line treat-
There are several different chemotherapeutic options for ment) were observed.93 Two large randomized phase III
patients with liver metastases from CRC. These treatment clinical trials are currently enrolling patients to evaluate
approaches are discussed elsewhere.72 Adjuvant therapy the benefit of adding radioembolization to standard
refers to systemic chemotherapy given after surgery to first-line chemotherapy regimens.
reduce the risk of recurrent disease. Neoadjuvant therapy
refers to preoperative systemic chemotherapy to reduce PERCUTANEOUS ABLATION
the risk of recurrence and/or downstage the disease to Patient selection, technical aspects of the procedure, and
allow for surgical resection. Often, systemic chemother- complications associated with the percutaneous ablative
apy is administered both before and after surgery and is therapies are discussed earlier. The published results of
referred to as a perioperative approach.72 percutaneous RFA of small (!5 cm) CRC metastases
compares well with postresection survival data.94 Also,
SURGICAL THERAPY emerging data concern the role of RFA in the palliation
Surgical resection is considered the only curative op- of CRC metastases. These data suggest a survival benefit
tion for patients with CRC metastases.72 Before being over systemic chemotherapy, which was previously the
considered for operation, it must be shown that the sole mainstay of therapy in these patients.95 Hepatic
patient has little or no extrahepatic disease and has metastases from CRC are also amenable to cryoablation
intrahepatic disease that can be safely resected. and microwave ablation, although there are fewer data
The goal of surgical resection is to remove all lesions to support their use. Many of the studies evaluating the
with tumor-free margins.89 For those patients who efficacy of cryoablation therapy do not separate patient
undergo resection for CRC metastases, the 5-year sur- population by type of neoplasm, making it more diffi-
vival approaches 45% to 60%.90,91 Combined modality cult to ascertain whether cryoablation is more or less
approaches such as surgical resection and intraopera- effective for specific tumor types.96
tive ablation, staged bilobar surgical resection, and
portal vein embolization with extended hepatectomy Neuroendocrine Liver Metastases
have all expanded the pool of surgical candidates
with CRC. Etiology and Natural History
Neuroendocrine tumors are relatively rare entities
CHEMOEMBOLIZATION with an estimated incidence of one or two cases per
Historically, patients who had unresectable colorectal 100,000 persons per year in the United States.97 They
cancer metastases that progressed on chemotherapy are a heterogenous group of neoplasms originating
were candidates for chemoembolization. A current area from endocrine cells. Thus, they can originate from
of research involves the use of irinotecan drug-eluting anywhere that endocrine cells live (e.g., gastrointesti-
beads to treat patients with CRC liver metastases. Irino- nal tract, pituitary, pancreas). Carcinoid, insulinoma, and
tecan is a chemotherapeutic agent that has been shown glucagonoma are just a few examples. Neuroendocrine
to increase survival and delay tumor progression when tumors also have a strong predilection for developing
added to the treatment regimen for patients with meta- liver metastases (up to 78% in some surgical series).98
static colorectal cancer. Initial results of a phase II clini- The tumors are generally slow growing and typically
cal trial reported an 80% response rate with reduction of have a long, indolent disease course, particularly when
contrast enhancement of treated tumors following treat- the tumor is of the nonfunctional type. Still, metastatic
ment.92 Other trials evaluating the safety and efficacy of neuroendocrine disease is associated with a 5-year
irinotecan drug-eluting beads in liver metastases from survival rate of only 22%.99
CRC are ongoing.
Clinical Features
RADIOEMBOLIZATION Patients clinical presentations usually result from the
Patients who have unresectable CRC metastases to the tumors biochemical activity or from local obstruction or
liver and are on systemic chemotherapy or have failed to infiltration of an adjacent anatomic structure.100 For ex-
respond to first- or second-line chemotherapeutic agents ample, a patient with a carcinoid tumor may present
are considered candidates for radioembolization.52 As with flushing, diarrhea, and weight loss.
24. INTERVENTIONAL ONCOLOGY 733
C D
FIGURE 24-10 Yttrium-90 (90Y) radiotherapy for colorectal liver metastases. A, Radionuclide scan following intraarterial injection of Tc-99m
macroaggregated albumin excludes significant shunting to the lungs. B, Celiac arteriography shows multiple vascular masses in the liver.
The cystic artery is identified (arrow). C, A coaxial microcatheter is used to select the artery, which is then embolized with coils. D, Inadvertent
delivery of 90Y to this site could lead to cholecystitis.
A B
tumors.105 Open or laparoscopic ablative therapies can symptoms caused by hormonal release immediately
be conducted at the time of surgical resection, allow- following therapy.106
ing treatment of the primary and metastatic lesions in Several studies have reported the beneficial therapeutic
one setting. effect of chemoembolization and bland hepatic emboliza-
tion for patients with metastatic neuroendocrine tumors.
LIVER DIRECTED THERAPY In a study published in 2007 comparing TACE with bland
Accepted indications for liver directed therapy are un- embolization, patients treated with TACE demonstrated a
resectable tumors with symptoms related to hormonal trend toward improvement in time to progression, symp-
excess and tumor bulk. The techniques of chemoembo- tom control, and survival.107 Likewise, published reports
lization and radioembolization are discussed previously of radioembolization in patients with metastatic neuroen-
in this chapter. An important adjunct to the preproce- docrine tumors have been favorable. Prolonged response
dure management of patients with neuroendocrine to treatment (i.e., #2 years) has been demonstrated.108
metastases is the administration of a somatostatin ana- Accordingly, the median survival was 70 months in a
logue before therapy whether the patient is currently retrospective review of 148 patients with metastatic neuro-
receiving this therapy or not. This measure should limit endocrine tumors treated with radioembolization.109
24. INTERVENTIONAL ONCOLOGY 735
PERCUTANEOUS ABLATION
KIDNEY PATIENT SELECTION Thermal ablation has emerged
as a treatment option for medically inoperable patients
Renal Cell Carcinoma with RCC. The early success with thermal ablation in this
population has provided an opportunity to treat patients
Etiology and Imaging who do not want to undergo surgery and those with
The American Cancer Society estimated 57,760 new underlying renal insufficiency, solitary kidney, trans-
cases of tumors of the kidney and renal pelvis with planted kidney, or multifocal tumors (e.g., individuals
12,980 deaths in the United States in 2009.111 Most of with von Hippel Lindau syndrome.)114 Biopsy of indeter-
these tumors will prove to be renal cell carcinoma minate renal masses may be obtained before or at the
(RCC). The expanding role of cross-sectional imaging same setting as thermal ablation. Biopsy is often not per-
in daily medical practice continues to increase the formed at a separate preablation setting because contro-
detection of incidental small renal masses.112 These versy exists over its utility for characterizing small renal
tumors classically present as a heterogeneously en- masses, thus limiting its value for clinical decision mak-
hancing mass that disturbs the renal contour. Multi- ing. The timing and role of biopsy with regard to ablation
phase contrast-enhanced imaging is typically used for is debated and more extensively reviewed elsewhere.115
staging purposes. Staging is performed with the TNM
staging classifications system that includes anatomic TECHNIQUE RFA and cryoablation are the primary
factors such as tumor size, venous invasion, renal cap- modalities used for percutaneous therapy of renal
sule invasion, adrenal involvement, and lymph node tumors.116 There has been a recent trend favoring cryoabla-
and distant metastasis.113 A unique characteristic of tion in the kidney although both methods have certain
this tumor is its tendency to spread in an intravascular advantages and disadvantages. A variety of imaging mo-
manner, along with the development of distant meta- dalities can be used, including ultrasound, CT, and MRI,
static lesions to the bone, brain, liver, and lungs. Even based largely on the interventionalists experience, avail-
though the imaging diagnosis of RCC is sometimes ability of equipment, and lesion location.116 Tumors less
straightforward by CT, problem-solving tools includ- than 4 cm in diameter (stage Ia) are most appropriate for
ing MRI and ultrasound are often needed. The Bosniak these ablative techniques. Ablation of larger tumors is fea-
classification system was developed as a means to sepa- sible, particularly if they are exophytic. Posterior exophytic
rate cystic renal masses into surgical and nonsurgical lesions are the most favorable; central and hilar lesions are
categories based on specific features. Much effort has much more difficult. Extrarenal complications are uncom-
been invested in developing methods to distinguish mon but may occur with anterior tumors (bowel or visceral
RCCs from complex renal cysts, angiomyolipomas, organ injury), central tumors (collecting system and main
oncocytomas, renal metastasis, and lymphoma. renal vessel injury), lower pole tumors (ureteral injury), or
At presentation, RCC is commonly asymptomatic and upper pole tumors (pleural effusion or pneumothorax).116
localized when detected. Whereas some studies advocate The procedure is most commonly performed under
watchful waiting and active surveillance, many patients CT, CT fluoroscopy, or ultrasound/fluoroscopic guid-
and physicians choose to treat these small, early stage ance. Ultrasound has the advantage of real-time moni-
tumors because there are less invasive options. Stage Ia toring during the ablation, whereas CT provides more
("4 cm) tumors represent the vast majority of lesions information about surrounding organs that must be
treated percutaneously or with nephron-sparing surgery. avoided.114 With the patient prone, scout CT images are
736 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
obtained for planning purposes. The anticipated route 159,390 lung cancer deaths for 2009, or 28% of all cancer-
may need to be altered due to differences in kidney posi- related deaths, and 219,440 new cases of lung cancer, or
tion from the supine diagnostic scan or phases of respi- 15% of cancer diagnoses.111 The World Health Orga-
ration. Hydrodissection may be employed if there is nization recognizes four major histologic subtypes:
need to displace nontarget structures. This technique adenocarcinoma including bronchioalveolar carcinoma,
entails needle placement and subsequent infusion of squamous cell carcinoma, large cell carcinoma, and small
either sterile water or dextrose 5% in water to separate cell carcinoma. Lung cancers are classified as either small
the target from nontarget structures. Saline solution cell (SCLC, 14% of cases) or nonsmall cell (NSCLC, 85%
should not be used for this purpose when performing of cases). SCLC is the more aggressive of the two types.
RFA, because the conductive properties of saline may Numerous environmental and lifestyle risk factors have
cause an unpredictable zone of ablation. A general been associated with lung cancer development, the most
guideline for probe placement is the 2 to 1 rule, in important being cigarette smoking, estimated to account
which probes should be placed no more than 2 cm apart for 90% of all lung cancers.111 Other risk factors include
from one another and within 1 cm of the tumor mar- radiation therapy, various environmental toxins, pulmo-
gin.114 Once the probes are in satisfactory position, one nary fibrosis, infection with human immunodeficiency
may proceed with ablation according to the manufac- virus, genetic factors, and possibly dietary habits. Present-
turers specifications and institutional protocol. With ing symptoms depend on the extent of disease. Chest
cryoablation, two freezing periods of 10 minutes are symptoms include cough, hemoptysis, chest pain, and
usually separated by an active thaw interval. Monitor- dyspnea. Many patients present with lymph node or sys-
ing images are obtained every 5 minutes during the temic involvement and are thus treated primarily with
freeze periods. After the second freeze, a passive or ac- chemotherapy and irradiation.
tive thaw is employed, the probes are removed, and final
imaging is obtained. Patients are recovered according to Imaging
the type of anesthesia/sedation they receive, observed Because of the typically late presentation and dismal
overnight, and discharged the following morning. prognosis of most lung cancer, concerted efforts are un-
derway in the United States and throughout the world to
RESULTS AND COMPLICATIONS Recovery is faster develop effective screening programs. Although many
after percutaneous ablation than with the laparoscopic pulmonary neoplasms are still discovered on conven-
approach. Thumar and colleagues114 recently summa- tional chest radiographs, CT and PET-CT have emerged
rized the results of RF ablation for RCC. At least 79% of as the diagnostic workhorses in the diagnosis and staging
tumors in all studies were treated in a single session. of lung cancer. In addition, CT is now commonly used to
After complete necrosis was achieved by imaging crite- guide percutaneous biopsy for tissue diagnosis.
ria, the local progression rates ranged from 0% to 9.7%.
Unfortunately, local progression was identified as late
Treatment
as 31 months after treatment, thus necessitating long-
term surveillance. In the same review, initial success THERMAL ABLATION
rates for cryoablation were reported as greater than 90% PATIENT SELECTION Most published research in pul-
in all series.114 The risk of local tumor progression ap- monary tumor ablation is related to treatment of NSCLC.
pears lower than with RF ablation, but the series are The primary scenario for percutaneous ablative therapy is
smaller and the follow-up periods shorter.114 For this the medically inoperable, high-risk patient with an early
reason, current follow-up strategies involve repeat CT stage lung cancer.117 This group typically includes patients
or MRI with and without contrast at 1, 3, 6, 12, 18, and who would normally qualify for surgical resection but will
24 months after ablation.115 not tolerate an operation due to an inadequate pulmonary
reserve or concomitant cardiopulmonary disease. Pulmo-
nary ablation can also be used in individuals with small
LUNG pulmonary metastases without hilar or mediastinal nodal
involvement or extrathoracic disease.117 Finally, palliative
Lung Cancer thermal ablation may be performed for patients experienc-
ing tumor related symptoms (e.g., painful chest wall
Etiology and Clinical Features masses). RFA should be avoided in the lung apex and
Lung cancer (bronchogenic carcinoma) refers to malig- mediastinum due to the risk of mechanical and thermal
nancies originating from the airway or pulmonary pa- injury.
renchyma. Primary lung cancer is the number one cause
of cancer-related deaths in men and women in the TECHNIQUE RFA or microwave ablation may inter-
United States. The American Cancer Society estimated fere with pacemaker or defibrillator function. Therefore,
24. INTERVENTIONAL ONCOLOGY 737
the interventionalist must consult with anesthesia or performed of 153 patients with 189 lesions who re-
cardiology services regarding the need for external ceived RFA and a median 20.5-month follow-up. The
pacing or defibrillation.117 Ablation may be done with Kaplan-Meier 1-, 2-, 3-, 4-, and 5-year survival rates for
midazolam and fentanyl, although some physicians pre- stage I nonsmall cell lung cancer were 78%, 57%, 36%,
fer monitored anesthesia or a general anesthetic. 27%, and 27%, respectively.117 Another group followed
Although some chest wall or pleural masses may be 60 patients with five or fewer tumors per patient with a
ablated with ultrasound guidance, the vast majority are diameter of less than 4 cm. Overall survival rates at 18
performed with CT guidance. A preprocedural CT should months were 76% for primary lung tumors and 71% for
be reviewed for planning purposes. The overlying skin is metastatic disease.117 Complications of percutaneous
prepped and local and extrapleural anesthesia is admin- lung ablation include postablation syndrome (see ear-
istered. A preliminary CT scan of the extrapleural needle lier discussion), bleeding, cardiopulmonary collapse,
is obtained to assess the potential trajectory of the probe pneumothorax, hemoptysis, pulmonary hemorrhage,
or electrode. The size and depth of the lesion determine reactive pleural effusion, bronchopleural fistula, infec-
the length and active tip of the probe selected.117 Treat- tion or abscess formation, damage to adjacent anatomic
ment times vary by ablative technology and number of structures, and skin burns during RFA secondary to
probes. After the lesion is treated, the probe is removed incorrect grounding pad placement.117
and a postprocedure CT scan is performed to evaluate
for pneumothorax. Postprocedure observation is per-
formed for 2 to 3 hours with a repeat chest radiograph to BONE
exclude pneumothorax.
Microwave ablation has many theoretical advantages Image-guided percutaneous treatment of bone tumors is
over other ablation systems, including the ability to another developing application of thermal ablation. In
achieve higher intratumoral temperatures, larger abla- some patients, it is an effective alternative to surgery or
tion volumes, and faster ablation times.118 In addition, external beam radiation. Percutaneous ablation is now
microwave ablation does not rely on an electrical circuit; the first line treatment for osteoid osteoma. It also has
as such, multiple probes may be used simultaneously. value in some other benign primary bone tumors and
The advantages of cryoablation over RFA include larger for palliation of painful bone metastases.121 Thermal
tumor ablation volumes, the ability to use multiple ablation can be combined with cementoplasty in metas-
probes, and less procedural pain. The ability to see tases at risk for fracture to provide stability as well as
lower attenuation ice as it covers a soft tissue mass is pain control.
also a consideration. When considering a musculoskeletal lesion for po-
tential ablation, a multidisciplinary approach should
IMAGING FOLLOW-UP There is no consensus re- be used with involvement of the medical oncologist,
garding the best imaging modality or surveillance proto- musculoskeletal-trained radiologist, and orthopedic
col after lung ablation. A common strategy involves CT oncologist to verify tumor type and choose the most
imaging at 1-, 3-, and then 6-month intervals. FDG PET- appropriate therapy. One should be familiar with the
CT has been recently shown to depict a higher number perilesional anatomy including adjacent nerves, blood
of treatment failures earlier than chest CT.119. The initial vessels, and organs.121 Additional tools such as motor-
postablation CT usually demonstrates a ground-glass evoked potentials may be used when lesions are near
opacity around the ablated mass which roughly equates the spinal cord or major motor nerves.121 Preprocedure
to the ablation margin.119 At 1 month, the lesion may planning requires an understanding of the lesion being
have apparently increased in size and appear as a treated. CT is the most commonly used modality for
nodular consolidation. Diminished or absent activity on skeletal ablation procedures because of the ability to
PET scans also suggests tumor necrosis without residual rapidly and accurately place devices. Ultrasound may
disease. Residual tumor is sometimes identified as up- be used in the setting of soft tissue tumor treatment.
take within the periphery of the lesion, although this
finding is not entirely specific.119
Osteoid Osteoma
RESULTS AND COMPLICATIONS The current litera- Osteoid osteoma is a small, painful, benign bone tumor
ture regarding thermal ablation of the lung involves that typically occurs in children and young adults. The
studies published with heterogenous groups with dif- classic presentation is severe pain that is worse at night
ferent follow-up periods and reporting standards.120 and is relieved with salicylates. Imaging demonstrates a
There is currently greater experience with RFA in that radiolucent nidus composed of vascular osteoblastic tis-
the majority of studies involving pulmonary ablation sue found primarily in the metaphysis and diaphysis
involve this technology. A retrospective review was of long bones.121 Effective treatment requires destruction
738 VI. NONVASCULAR AND ONCOLOGIC INTERVENTIONS
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