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Chapter12:Embolization of livertumors
http://internalmedicinebook.com
10. Covey AM, Brody LA, Maluccio MA, etal. Variant hepatic
arterial anatomy revisited:Digital subtraction angiography
performed in 600 patients. Radiology 2002; 224:542–547.
11. Couinaud C. Liver anatomy:Portal (and suprahepatic) or biliary
segmentation. Dig Surg 1999; 16:459–467.
12. Mlakar B, Gadzijev EM, Ravnik D, etal. Anatomical variations
of the arterial pattern in the right hemiliver. Eur J Morphology
2002; 40:267–273.
13. Mlakar B, Gadzijev EM, Ravnik D, etal. Anatomical variations
of the arterial pattern in the le hemiliver. Eur J Morphology
2002; 40:115–120.
14. Couinaud C. Le foie:Études anatomiques et chirurgicales. Paris,
France:Masson, 1957; pp.9–12.
15. Fasel J, Selle D, Evertsz C, etal. Segmental anatomy of the
liver:Poor correlation with CT. Radiology 1998; 206:151–156.
16. Lee HY, Chung JW, Park JH, etal. A new and simple
practical plane dividing hepatic segment 2 and 3 of the
liver:Evaluation of its validity. Korean J Radiol 2007;
8:302–310.
17. Song SY, Chung JW, Lim HG, etal. Nonhepatic arteries
originating from the hepatic arteries:Angiographic analysis in
250 patients. J Vasc Interv Radiol 2006; 17:461–469.
18. Hashimoto M, Heianna J, Tate E, etal. e feasibility of
retrograde catheterization of the right gastric artery via the le
gastric artery. J Vasc Interv Radiol 2001; 12:1103–1106.
19. Nakamura H, Uchida H, Kuroda C, etal. Accessory le gastric
artery arising from le hepatic artery:Angiographic study. AJR
Am J Roentgenol 1980; 134:529–532.
20. Chuang PV, Wallace S, Stroehlein J, etal. Hepatic artery
infusion chemotherapy:Gastroduodenal complications. AJR Am
J Roentgenol 1982; 137:347–350.
21. Williams DM, Cho KJ, Ensminger WD, etal. Hepatic falciform
artery:Anatomy, angiographic appearance, and clinical
signicance. Radiology 1985; 156:339–340.
22. Bianchi HF, Albanese EF. e supraduodenal artery. Surg Radiol
Anat 1989; 11:37–40.
23. Daseler EH, Anson BJ, Hambley WC, etal. e cystic artery and
constituents of the hepatic pedicle:Astudy of 500 specimens.
Surg Gynecol Obstet 1947; 85:47–63.
24. Lie DM, Salem R, Bui JT, etal. Angiographic considerations in
patients undergoing liver-directed therapy. J Vasc Interv Radiol
2005; 16:911–935.
25. Tohma T, Cho A, Okazumi S, etal. Communicating arcade
between the right and le hepatic arteries:Evaluation with CT
and angiography during temporary balloon occlusion of the
right or le hepatic artery. Radiology 2005; 237:361–365.
26. Stapleton GN, Hickman R, Terblanche J. Blood supply of the
right and le hepatic ducts. Br J Surg 1998; 85:202–207.
27. Kim HC, Chung JW, Lee W, etal. Recognizing extra-hepatic
collateral vessels that supply hepatocellular carcinoma to avoid
complications of transcatheter arterial chemoembolization.
Radiographics 2005; 25:S25–S39.
28. Chung JW, Kim HC, Jae HJ, etal. Transcatheter arterial
chemoembolization of hepatocellular carcinoma:Prevalence
and causative factors of extrahepatic collateral arteries in 479
patients. Korean J Radiol 2006; 7:257–266.
29. Michels NA. Collateral arterial pathways to the liver aer
30. Chung JW, Park JH, Han JK, etal. Transcatheter oily
chemoembolization of the inferior phrenic artery in
hepatocellular carcinoma:e safety and potential therapeutic
role. J Vasc Interv Radiol 1998; 9:495–500.
31. Miyayama S, Matsui O, Taki K, etal. Extrahepatic blood supply
to hepatocellular carcinoma:Angiographic demonstration and
transcatheter chemoembolization. Cardiovasc Intervent Radiol
2006; 29:39–48.
32. Nakai M, Sato M, Kawai N, etal. Hepatocellular
carcinoma:Involvement of the internal mammary artery.
Radiology 2001; 219:147–152.
33. Miyayama S, Matsui O, Akakura Y, etal. Hepatocellular
carcinoma with blood supply from omental branches:Treatment
with transcatheter arterial embolization. J Vasc Interv Radiol
2001; 12:1285–1290.
34. Miyayama S, Matsui O, Nishida H, etal. Transcatheter arterial
chemoembolization for unresectable hepatocellular carcinoma
fed by the cystic artery. J Vasc Interv Radiol 2003; 14:1155–1161.
35. Kim HC, Chung JW, Park JH, etal. Transcatheter arterial
chemoembolization for hepatocellular carcinoma:Prospective
assessment of the right inferior phrenic artery with C-arm CT.
J Vasc Interv Radiol 2009; 20:888–895.
36. Kim HC, Chung JW, An S, etal. Le inferior phrenic artery
feeding hepatocellular carcinoma:Angiographic anatomy using
C-arm CT. AJR Am J Roentgenol 2009; 193:W288–W294.
37. Kim HC, Chung JW, Jae HJ, etal. Hepatocellular
carcinoma:prediction of blood supply from an internal
mammary artery with multi-detector row CT. J Vasc Interv
Radiol 2008; 19:1419–1425.
38. Kim HC, Chung JW, Lee IJ, etal. Intercostal artery supplying
hepatocellular carcinoma:Demonstration of a tumor feeder
by C-arm CT and multidetector row CT. Cardiovasc Intervent
Radiol 2011; 34:87–91.
39. Miyayama S, Matsui O, Akakura Y, etal. Use of a catheter with
a large side hole for selective catheterization of the inferior
phrenic artery. J Vasc Interv Radiol 2001; 12:497–499.
40. Baek JH, Chung JW, Jae HJ, etal. A new technique for
superselective catheterization of arteries originating from a
large artery at an acute angle:Shepherd-hook preshaping of
a micro-guide wire. Korean J Radiol 2007; 8:225–230.
41. Miyayama S, Matsui O, Taki K, etal. Transcatheter arterial
chemoembolization for hepatocellular carcinoma fed by the
reconstructed inferior phrenic artery:Anatomical and technical
analysis. J Vasc Interv Radiol 2004; 15:815–823.
42. Sakamoto I, Aso N, Nagaoki K. Complications associated
with transcatheter arterial embolization for hepatic tumors.
Radiographics 1998; 18:605–619.
43. Kim HC, Chung JW, Choi SH, etal. Hepatocellular carcinoma
supplied by the internal mammary artery:Angiographic
anatomy in 97 patients. Radiology 2007; 242:925–932.
44. Kim HC, Chung JW, An S, etal. Transarterial
chemoembolization of a colic branch of the superior mesenteric
artery in patients with unresectable hepatocellular carcinoma.
J Vasc Interv Radiol 2011; 22:47–54.
45. Chung JW, Park JH, Han JK, etal. Hepatic tumors:predisposing
factors for complications of transcatheter oily
chemoembolization. Radiology 1996; 198:33–40.
ligation of the hepatic artery and removal of the celiac axis.
Cancer 1953; 6:708–724.
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Chapter
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Conventional chemoembolization and
chemoembolization with drug-eluting
13
beads:Technique and future potential
Julius Chapiro, Florian Nima Fleckenstein, Lynn Jeanette Savic, and
Jean-François H. Geschwind
Background
With increasing incidences, primary liver cancer is already
the third most common cause of cancer-related deaths.1
Most liver cancer patients are diagnosed at intermediate
to advanced stages and only 20–30% of them are primarily
amendable for potentially curative surgical therapies.2 is
circumstance provides the clinical need for alternative therapeutic approaches that would be able to control the disease
with the goal of potentially increasing the overall survival
upon diagnosis.
Since the 1970s, catheter-based intra-arterial therapies
consistently gained acceptance throughout modern medical science. Nowadays, transarterial approaches constitute a
core element of established therapies of liver malignancies.
In this regard, conventional transarterial chemoembolization (cTACE) is one of the most frequently used techniques.
TACE with drug-eluting beads (DEB-TACE) is a fairly new
technique that was presented to the majority of interventional oncologists about 10years ago. e main objectives
of both approaches are to provide therapeutic options for
non-resectable patients in order to improve survival and
quality of life in a palliative setting, as well as downstaging or
bridging and thus making patients amenable for potentially
curative surgical treatment.2 Both cTACE and DEB-TACE
exploit the biological characteristic of most hepatic malignancies being supplied by arterial blood. In contrast, healthy liver
tissue is mostly supplied through the portal vein. By injecting
chemotherapeutic agents into the tumor-feeding vessels, both
procedures target tumor tissue while sparing the surrounding
liver parenchyma.
In this chapter, we will describe indications, techniques,
and complications of cTACE and DEB-TACE and provide the
reader with an overview of the scientic rationale. As a conclusion, we will give a brief outlook on future developments.
3,4
Concept and materials used duringTACE
e general concept of cTACE was introduced in 1977 by Yamada
etal., who intra-arterially delivered gelatin sponge pieces permeated with mitomycin C or Adriamycin, aer superselecting
the tumor-feeding artery of unresectable hepatomas.
40years later, the general concept of cTACE remains the same:a
mixture of chemotherapeutic agents combined with an oil-based
contrast medium (Lipiodol Ultrauide) is selectively delivered
to the tumor-feeding artery. is is followed by a temporary
or permanent embolization (Figure 13.1). e dual character
of Lipiodol, serving as a drug carrier and an embolizing agent,
makes it a key ingredient of cTACE.
5,6
It is selectively taken up
by tumor tissue. Persisting within the tumor for several weeks,
Lipiodol embolizes the tumor vasculature up to the capillaries.
Regarding the mixture of chemotherapeutic agents,
single-drug therapy and combination chemotherapy have been
used during chemoembolization. In the USA, doxorubicin is
mostly used as a single-drug therapy for DEB-TACE; the most
common drug combination used for cTACE is the combination of cisplatin, doxorubicin, and mitomycin C.9 However, due
to the currently reduced availability of cisplatin, most centers
rely on the combination of doxorubicin and mitomycin. e
admission of an additional embolic agent (Gelfoam, polyvinyl
alcohol (PVA) particles, or trisacryl gelatin microspheres) aer
the application of Lipiodol and the chemotherapeutic agent
causes stasis and prevents a potential washout of the previously
injected drug–Lipiodol cocktail.
10
As opposed to cTACE, DEB-TACE substitutes Lipiodol
as the drug-carrying medium with polymer-based microspheres. Thus, it allows a more targeted drug delivery to
the tumor, while further reducing the systemic drug exposure (Figure13.1).11 As a result, there has been a growing
interest in using DEB-TACE to treat patients’ hepatic malignancies, especially in the USA and Europe.7 LC Beads (DC
3,4
Nearly
7,8
Interventional Oncology, Second Edition, ed. Jean-François H. Geschwind and Michael C. Soulen. Published by Cambridge University Press.
©Cambridge University Press2016
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Patient selection and contraindications for TACE and DEB-TACE
100 µm
DEB-TACEcTACE
100 µm
embolic
agent
Figure 13.1 Schematic diagram of the mechanism of action of conventional
transarterial chemoembolization (cTACE) and drug-eluting bead transarterial
chemoembolization (DEB-TACE). Top: cTACE. A mixture of chemotherapeutic
agents combined with an oil-based contrast medium (Lipiodol) is selectively
delivered to the tumor-feeding artery. Embolizing the tumor vasculature up to
the capillaries allows the uptake of chemotherapeutic agents into the tumor.
Bottom: DEB-TACE. Polymer-based microspheres deliver the chemotherapeutic
agents to the tumor, while reducing the systemic drug exposure. Depending
on the size of the beads, tumor vessels more proximately or distally are
occluded, while the chemotherapeutic agents affect the tumor.
drug-eluting
bead
drug lipiodol
Copyright © 2014 by Lynn Jeanette Savic
Beads in Europe; Biocompatibles/BTG) and QuadraSpheres
(Hepaspheres in Europe; Merit Medical Systems) are the two
major types of drug-eluting microspheres available in the
USA. Both have not yet been fully approved by the Food
and Drug Administration (FDA) as drug carriers; however, they are fully approved as embolic agents.11 Most of
the clinical data has been generated with LC Beads. This
device is made of non-biodegradable materials, such as
PVA hydrogel that has been modified by the addition of
sulfonic acid-containing components. The microspheres
can be loaded with doxorubicin or irinotecan, ranging in
size from 75 to up to 900µm.12 In general, the smaller the
size of the bead diameters, the more distally they can penetrate into the tumor and occlude its vessels. Accordingly,
smaller bead diameters are likely to cause a more extensive
necrosis.13 The maximum loading capacity for doxorubicin
is defined by the manufacturer as 40mg/mL hydrated LC
Beads; thus a loading of 25mg/mL was recommended out
of technical considerations.14 It has been stated in histopathological analysis that DEB-mediated drug delivery and
release to the tumor tissue cause local coagulative necrosis
and an inflammatory-fibrotic tissue and are therefore highly
efficient.
15
e other types of microspheres (QuadraSphere/Hepasphere
microspheres) consist of superabsorbent polymer, a hydrophilic and highly absorbent material that is non-biodegradable.
ese spheres have the ability to absorb uids and to expand
their volume to a size of up to 800µm. ese microspheres can
be loaded with doxorubicin, epirubicin, and cisplatin.
16
To date, cTACE is the preferred treatment for palliation of unresectable hepatocellular carcinoma (HCC).
17–19
Furthermore, it
is successfully used as an adjunctive therapy to liver resection
or as a bridge to liver transplantation, as well as prior to or aer
radiofrequency ablation.
20–24
Other palliative applications of
TACE include unresectable cholangiocarcinomas,25 carcinoid
and pancreatic islet cell tumors, and sarcomas metastatic to
the liver.
26,27
Similarly, DEB-TACE has been successfully used
in patients with unresectable HCC, cholangiocarcinoma, neuroendocrine tumors, and hepatic colorectal metastases.
28–30
Generally, it can be noted that chemoembolization is indicated
for liver-dominant, non-resectable malignancies. In this context, it has been ocially included in the guidelines for the treatment of patients with intermediate-stage HCC. Furthermore it
is now an integral part of the commonly used Barcelona Clinic
Liver Cancer (BCLC) staging system.31 However, not all patients
with unresectable primary liver tumors will benet from
chemoembolization. One important aspect in the selection of
patients is the presence of adequate liver function. In patients
with advanced liver disease, treatment-induced liver failure
may oset the survival benet of the intervention. Predictors
of outcome are related to tumor burden (tumor size, vascular
invasion, and alpha-fetoprotein levels), the functional impairment of the liver (Child–Pugh, bilirubin, ascites), performance
status (Karnofsky index, Eastern Cooperative Oncology Group
(ECOG) performance score), and extrahepatic spread. Overall,
the best candidates are patients with preserved liver function
and asymptomatic lesions without vascular invasion or extrahepatic spread.
32
Table13.1 summarizes the list of absolute and relative con-
traindications for TACE and DEB-TACE. Due to the paucity of
reliable clinical data, the exclusion criteria for DEB-TACE are
more extensive than forcTACE.
Technique
TACE and DEB-TACE procedures share a common approach.
Initially, several diagnostic angiograms are performed to identify the hepatic arterial anatomy, the tumor-feeding vessels and
arteriovenous shunts (Figure13.2 and Figure 13.3). Aceliac
angiogram may adequately demonstrate hepatic branch anatomy, or variant arteries, such as the presence of replaced le
hepatic artery. Whenever possible, the right inferior phrenic
artery should be examined to exclude malignant parasitization of blood ow. It is necessary that the injection rates used
balance adequate opacication of the targeted vessels without unnecessary reux of contrast material into the aorta or
other vessels proximal to the injection site. Depending on the
tumor location, a selective hepatic arteriogram demonstrates
the tumor “blush” (Figure 13.4). Special attention should be
paid to the falciform, phrenic, right, or accessory gastric arteries and to the supraduodenal, retroduodenal, retroportal, and
cystic arteries, so as to avoid non-target embolization. In difcult cases with complex vascular anatomy, the utilization of
three-dimensional (3D) rotational angiography may help in
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AB C
Figure 13.2 Digital subtraction angiography (DSA) anteroposterior views of the superior mesenteric artery, celiac axis, and selective accessory right hepatic
artery in a 55-year-old male patient with unresectable multifocal hepatocellular carcinoma treated with transarterial chemoembolization. (A) Accessory right
hepatic artery arising off the superior mesenteric artery, supplying multiple lesions. (B) DSA of the celiac axis demonstrates the presence of a right hepatic artery.
(C) Selective angiogram of the accessory right hepatic artery, showing two hypervascular lesions.
Table 13.1 Contraindications for transarterial chemoembolization (TACE)
A
Absolute
contraindications Relative contraindications
• Tumor resectability
• Untraceable systemic
infection
• Uncorrectable bleeding
disorder
• Uncorrectable contrast
sensitivity
• Leukopenia (white
blood cell count 1000/
μL)
• Cardiac or renal
insufficiency
• Hepatic encephalopathy
• ECOG performace
status 3
a
Specific contraindication for drug-eluting beads TACE (DEB-TACE).
ECOG = Eastern Cooperative Oncology Group; BCLC = Barcelona Clinic for
Liver Cancer.
minimizing procedure risks or complications and lead to more
eective lesion targeting.
• Biliary obstruction
• Serum bilirubin 3 mg/dL
• BCLC class C (vascular invasion including
segmental portal obstruction)
a
• Lactate dehydrogenase 425 U/L
• Aspartate aminotransferase 5× higher
than the upper limit of normal
• Tumor burden involving >50% of
a
the liver
• Extrahepatic metastases
• Mild or severe ascites
a
• Recent variceal bleeding
• Thrombocytopenia
• Intractable arteriovenous fistula
• Surgical portocaval anastomosis
33
B
In the following, we will describe the Yale University School
of Medicine protocol for cTACE and DEB-TACE using LC
Bead microspheres.
During the cTACE procedure, patients are usually treated
with selective (lobar or segmental) or superselective injections. e cocktail of chemotherapeutic agents used is a double mixture of 50mg doxorubicin and 10mg mitomycin C
in a 1:1 mixture with Lipiodol (Guerbet, France). is is followed by an application of 15–20mL of arterial lidocaine for
Figure 13.3 Digital subtraction angiography (DSA) anteroposterior views
of the celiac axis, superior mesenteric artery, and right hepatic artery of a
71-year-old male patient with hepatocellular carcinoma. (A) DSA view of
the celiac axis, showing little hepatic perfusion. (B) DSA view of the superior
mesenteric artery showing a replaced right hepatic artery.
immediate analgesia and prevention of postprocedural symptoms. Finally, 3–6mL of 100–300µm diameter microspheres
(Embospheres, Merit Medical, South Jordan, UT, USA), suspended in a 1:1 ratio of contrast medium, is injected to achieve
arterial ow reduction. e grade of arterial occlusion can be
measured by counting the number of heart beats it takes to
wash out the contrast media aer the TACE procedure (2–5
being ideal).
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Figure 13.4 T1-weighter contrast-
enhanced MRI of a patient with a single
hypervascular hepatocellular carcinoma
(HCC) lesion on baseline (A) as well as
one month after drug-eluting beads
transarterial chemoembolization (B). The
result demonstrates a good tumor response
with extensive central tumor necrosis and
minimal residual tumor rim enhancement.
The images below (C and D) demonstrate
a T1-weighted, contrast-enhanced MRI
in another patient with bi-focal HCC
before and after conventional transarterial
chemoembolization (cTACE). An almost
complete devascularization of the lateral
lesion is evident on the follow-up MRI image
(D), a hemorrhagic component is apparent
in the more medially located lesion.
e DEB-TACE procedure at Yale New Haven Hospital,
Yale University School of Medicine is being performed in agreement with the results of a consensus meeting held during the
European Conference on Interventional Oncology in 2012.15
Injections are usually selective to superselective (segmental or
even subsegmental). Prior to the procedure, LC Beads (2mL,
Biocompatibles/BTG, Surrey, United Kingdom) with a diameter of 100–300µm are loaded with 100mg doxorubicin hydrochloride (25mg/mL) in the oncological pharmacy. Aerwards
they are mixed with an equal volume of non-ionic contrast
medium and le for 2–3minutes to become a homogeneous
mixture. Up to 4mL of DEBs is injected until complete delivery
or the ow of the feeding vessel declines.
It is important to note that the injection of DEBs should be
performed very carefully and under uoroscopic guidance to
prevent reux. Sedimentation of the mixture can be avoided by
rotating the syringe while applying the loaded DEBs. Arterial
ow reduction is the technical endpoint of the DEB-TACE procedure, while complete occlusion of the vessel must be avoided.
It is absolutely crucial to preserve an arterial pathway for a
retreatment, since repeated sessions are recommended and
usually needed.
for a clinical follow-up 4–6 weeks aer treatment. During
this follow-up examination, a liver function test, as well as a
perfusion–diusion magnetic resonance imaging (MRI) scan
of the liver, is performed (Figure13.4). Decisions to re-treat
are based upon the combination of imaging and laboratory
ndings as well as the patient’s clinical performance status.
Although overall survival continues to be the ultimate endpoint of clinical cancer research, most trials rely on imaging
biomarkers in order to assess local tumor status as well as to
compare the ecacy of dierent intra-arterial modalities.
e primary clinical purpose of follow-up imaging, however,
remains a reliable and early identication of non-responders in
order to then subject these patients to retreatment.
Over the last two decades, tumor response criteria have
come a long way from purely size-based, anatomic methods
such as the Response Evaluation Criteria in Solid Tumors
(RECIST) and the World Health Organization (WHO)
guidelines towards more functional, enhancement-, and
diusion-based parameters with a strong emphasis on MRI
as the ultimate imaging modality. is trend is based on the
mechanism of most intra-arterial therapies that involves the
element of embolization in order to induce tumor infarction, which, in return, leads to tissue necrosis without
Follow-up and evaluation of response to treatment
e assessment of tumor response of hepatic malignancies aer intra-arterial therapies is of major clinical interest.
For maximum benet, patients should be advised to return
immediate eects on the overall lesion size. Because of that,
enhancement-based response criteria such as the European
Association for the Study of the Liver (EASL) guideline as
well as modied RECIST (mRECIST) have become increasingly popular and were shown to represent tumor pathology
more accurately as compared to RECIST.34 However, these
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techniques have considerable limitations because of their limited reproducibility as well as their inability to evaluate entire
lesions, which makes them inevitably inaccurate in predicting
the true extent of the mostly heterogeneous, posttherapeutic
tumor necrosis.
35
e narrow applicability of the above-mentioned techniques provided the rationale for the development of new,
3D quantitative assessment techniques for tumor response
aer transarterial chemoembolization as well as other
catheter-based intra-arterial therapies. As a rst milestone, a
goal was to develop and to validate a workow-ecient tumor
segmentation technique, which would address the issue of
accuracy and clinical practicability. e competing concepts
of fully automated tumor segmentation vs. a semiautomated
technique were tested and the latter was identied as a more
can be reduced further by superselective chemoembolization,
as opposed to non-selective lobar embolization.
41
By using DEB-TACE, systemic toxicities can be signicantly reduced. In fact, peak plasma concentrations of doxorubicin are nearly undetectable aer DEB-TACE procedure.42
However, adverse eects of doxorubicin include alopecia and
skin discoloration to mucositis and bone marrow suppression. Amulticenter, randomized, prospective phase II trial,
investigating toxicity proles of cTACE and DEB-TACE in
HCC patients, conrmed that DEB-TACE is better tolerated
regarding the frequency and severity of treatment-related
adverse eects. Only 11.8% of patients treated with DEB-TACE
revealed the presence of signicant events, whereas 25.9% of
patients aer cTACE experienced treatment-related adverse
43
eects.
accurate and clinically intuitive approach, primarily because it
allowed for a radiological reader to modify the enclosed liver
tumor volume.36 Because of the 3D quantitative character of
this technique, this method has been referred to as volumetric
(v)RECIST. e need for new 3D quantitative approaches that
would encompass the functional parameters of liver tumors
led to the advent of two additional MR-based parameters,
the quantitative (q)EASL as well as the quantitative apparent
diusion coecient (qADC). Both techniques are anchored
in a region-of-interest (ROI)-based voxel-by-voxel analysis
and quantication of the brightness signal, which allows for
a whole-tumor analysis. ese techniques provide the radiological reader with a precise quantication of the enhancing
or diusion-restricted tumor portions and were shown to provide an accurate correlation with tumor pathology, as seen on
tumor explants.37 Recent studies have also conrmed the intuitive advantages of these techniques over the non-3D methods
in predicting survival in both primary and secondary liver cancer.38 However, a major drawback continues to be the necessity
of dedicated soware, which would allow for a dissemination
of these techniques beyond academic institutions. In summary,
new 3D quantitative tumor assessment techniques continue to
be a hot topic of clinical research in interventional oncology
and the great wealth of knowledge that has been added over
the last decade continues to grow. Afuture development might
very well be the inclusion of 3D quantitative tumor analysis techniques into novel staging systems in order to nally
achieve the perfect symbiosis between periprocedural imaging
with intraprocedural treatment decisions.
39
Complications and side eects
e overall safety of TACE has been investigated by a number of trials. As for systemic adverse eects, nausea, vomiting,
bone marrow aplasia, renal failure and potentially cardiac toxicity have been reported. In approximately 10% of patients, the
self-limiting postembolization syndrome occurs. It includes
nausea, vomiting, fever, right upper quadrant pain, and
increased white blood cell count. It is caused by tumor necrosis, acute cytokine release, and systemic exposure to chemotherapeutic agents.40 Severe complications, such as liver abscess
or failure, cholecystitis, biloma, and hemorrhage, are rare and
Clinical outcome
In 2002 two prospective phase III trials showed a clear survival
benet for HCC patients treated with cTACE over patients
treated with best supportive care.
vide level 1 evidence, which led to the inclusion of cTACE to
the ocial treatment guidelines for HCC. Furthermore, they
helped establish the BCLC staging system. Ameta-analysis that
included seven randomized trials of arterial embolization for
unresectable HCC showed the ecacy of cTACE. Compared
to control (either conservative treatment or less favorable therapy, such as intravenous 5-uorouracil), there was a statistically signicant improvement in 2-year survival aer arterial
chemoembolization.21 e median overall survival of patients
with inoperable HCC is 4–7months (which can be extended
with maximal supportive care to approximately 10months).
cTACE showed a median overall survival of up to 2years and,
although rarely, converted some patients into operable candidates. In regard of the treatment of hepatic metastases, there is
less experience with cTACE.27 However, several reports show
an excellent symptomatic and biologic complete response rate
of 70–73%.44 e ecacy of cTACE in other groups, such as
patients with colorectal metastasis, is less established and will
be discussed further within the respective chapter.
e introduction of DEB-TACE has led to a number of
studies investigating the eciency of this new drug delivery approach. In 2009 an FDA-sanctioned prospective
phase II pilot study evaluated safety and ecacy as well as
progression-free survival and overall survival in 20 mostly
cirrhotic (80%) patients with unresectable HCC. e majority of the treated patients were staged as Child–Pugh A(75%),
while 12 patients (60%) were classied as BCLC stage C.Aer
a total of 34 sessions, 64% of the patients were classied as
responders and 30% achieved complete response according to
EASL criteria. Aer 6months, only 1patient showed progressive disease according to RECIST. e median overall survival of 26months in a majority of advanced patients (BCLC
C) conrmed the potential of DEB-TACE as benecial over
cTACE.
46
e PRECISION V study, a multicenter, prospective, randomized phase II trial, had the goal of comparing the safety
18,19
ese large studies pro-
45
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Chapter13:Chemoembolization technique and future potential
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and ecacy of cTACE with those of DEB-TACE. Although
complete response rates aer 6months were almost identical (26.6% and 22.2% in the DEB-TACE and cTACE groups,
respectively), patients in the DEB-TACE group showed better imaging response to treatment according to EASL criteria than those in the cTACE group. Furthermore, the rate of
progressive disease was signicantly lower in the DEB-TACE
than in the cTACE group (32.3% vs. 40.7%).43 With regard
to long-term outcomes, one retrospective study including 71
unresectable HCC patients, 63% of whom were treated with
DEB-TACE and 37% treated with cTACE, reported a median
overall survival of 610 days in the DEB-TACE group vs.
284days aer cTACE. However, due to the highly heterogeneous groups and a lack of strict inclusion criteria, the results
of this study must be interpreted with caution. Conventional
TACE continues to be the gold standard, since more prospective randomized trials will be needed to deliver denitive data
on patient survival before DEB-TACE can be fully included in
the ocial guidelines.
Combination therapies
eoretically, embolization of the tumor-feeding vessel should
cause ischemia of the entire tumor. Specically in combination
with systemic chemotherapy, it should result in complete tumor
necrosis. However, partial response and tumor recurrence
represent major clinical problems aer chemoembolization.
e mechanisms involved are not yet completely understood.
Animal studies have shown that tumor ischemia and tissue
hypoxia may upregulate several molecular factors, such as the
vascular endothelial growth factor (VEGF) through the hypoxia
inducible factor-1 (HIF-1), thereby preventing cell apoptosis and
stimulating tumor growth.
47,48
In this context, a combination of
antiangiogenic agents and chemoembolization seems reasonable. As such, a prospective, randomized, placebo-controlled trial
has conrmed that sorafenib, a multikinase inhibitor with strong
antiangiogenic properties, signicantly prolonged survival of
patients with HCC, making it the only FDA-approved drug for
systemic chemotherapy of HCC.49 Several trials have already
been completed and some are still ongoing in order to assess
the ecacy of a combination of sorafenib and chemoembolization. As such, a single-center prospective phase II study including 35 patients with unresectable HCC was designed to evaluate
the safety and ecacy of DEB-TACE combined with sorafenib.
Patients were treated on a 6-week cycle regimen, in which one
cycle consisted of 400mg sorafenib twice a day, initiated 1week
the fact that sorafenib was given continuously throughout the
planned DEB-TACE treatments. Most other trials used sorafenib
sequentially in order to reduce potential toxicities, yet a simultaneous application of the drug with TACE delivers the antiangiogenic eects when they are needed the most. Concerning the
secondary endpoint of this trial, the published data also demonstrated promising survival outcomes. Results from a large
non-randomized observational registry study (GIDEON trial)
undertaken to evaluate the safety of sorafenib in patients with
unresectable HCC in clinical practice rearm the safe use of
sorafenib in the context of TACE. e study also demonstrates
better overall survival in patients treated with sorafenib and
concomitant TACE compared with non-concomitantly treated
patients.51 Currently, there are several ongoing randomized,
double-blinded controlled multicenter trials that might provide
data on overall survival rates for sorafenib in combination with
TACE. e results of those trials should be available at the end
of2016.
Conclusion and outlook
cTACE and DEB-TACE are routinely performed in many institutions throughout the world. e number of intra-arterial
treatments is likely to further increase in the coming years.
Local application of chemotherapeutics and the induction of
ischemia while sparing systemic toxicities are the two central
antitumor eects of both approaches. Despite the superior data
of DEB-TACE concerning local tumor response and toxicity
levels, cTACE remains the gold standard for the treatment of
hepatic neoplasms, as a clear survival benet in patients treated
with DEB-TACE could not be shown untiltoday.
In the future, the goal of new developments will be the
maximization of eciency of chemoembolic treatments and
further reducing systemic adverse eects. Although tumor
response assessment by novel 3D quantitative approaches36
and advanced functional imaging52 has been successfully introduced, standardization of those methods will be challenging. Furthermore, advanced intraprocedural imaging such as
dual-phase cone-beam computed tomography will help predict tumor response immediately aer treatment.53 Finally,
the combination of systemically applicable targeted agents and
intra-arterial therapies will continue to be studied in greater
detail. Taken together, all those eorts will likely lead to new
treatment guidelines, a new standard of care for liver cancer
patients and a potentially improved overall survival for patients
in a palliative setting.
before DEB-TACE. All patients received DEB-TACE treatment
and the dose of doxorubicin decreased over time (cycle 1:75mg;
cycle 2:60mg; cycle 3:49 mg). e study’s primary endpoints
were safety and toxicity and the secondary endpoint was ecacy.
All patients experienced at least one treatment-related toxicity
during cycle 1.However, most adverse eects were minor and
only 17% of all toxicities were grade 3–4. Using EASL criteria, tumor response rate was 58% and the disease control rate
100%, with no patient showing tumor progression. is study
was the rst to conrm the safety prole of the DEB-TACE/
sorafenib combination.50 What makes this study truly unique is
References
1. Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics,
2002. CA Cancer J Clin 2005; 55:74–108.
2. Otto G, Schuchmann M, Hoppe-Lotichius M, etal. How
to decide about liver transplantation in patients with
hepatocellular carcinoma:size and number of lesions or
response to TACE? J Hepatol 2013; 59 (2):279–284.
3. Yamada R, Nakatsuka H, Nakamura K, Sato M, Itami M,
Kobayashi N, etal. Hepatic artery embolization in 32 patients with
unresectable hepatoma. Osaka City Med J 1980; 26 (2):81–96.
125
Section III:Primary liver cancers
http://internalmedicinebook.com
4. Yamada R, Sato M, Kawabata M, Nakatsuka H, Nakamura K,
Takashima S. Hepatic artery embolization in 120 patients with
unresectable hepatoma. Radiology 1983; 148 (2):397–401.
5. Nakakuma K, Tashiro S, Hiraoka T, Uemura K, Konno T,
Miyauchi Y, etal. Studies on anticancer treatment with an oily
anticancer drug injected into the ligated feeding hepatic artery
for liver cancer. Cancer 1983; 52 (12):2193–2200.
6. Konno T, Maeda H, Iwai K, Tashiro S, Maki S, Morinaga T,
etal. Eect of arterial administration of high-molecular-weight
anticancer agent SMANCS with lipid lymphographic agent on
hepatoma:a preliminary report. Eur J Cancer Clin Oncol 1983;
19 (8):1053–1065.
7. Pleguezuelo M, Marelli L, Misseri M, etal. TACE versus TAE
as therapy for hepatocellular carcinoma. Expert Rev Anticancer
er 2008; 8 (10):1623–1641.
8. Yumoto Y, Jinno K, Tokuyama K, etal. Hepatocellular
carcinoma detected by iodized oil. Radiology 1985; 154
(1):19–24.
9. Liapi E, Geschwind JF. Transcatheter arterial
chemoembolization for liver cancer:is it time to distinguish
conventional from drug-eluting chemoembolization? Cardiovasc
Intervent Radiol 2011; 34:37–49.
10. Brown DB, Gould JE, Gervais DA, etal. Transcatheter therapy
for hepatic malignancy:standardization of terminology
and reporting criteria. J Vasc Interv Radiol 2009; 20 (7
Suppl.):S425–S434.
11. Hong K, Khwaja A, Liapi E, Torbenson MS, Georgiades CS,
Geschwind JF. New intra-arterial drug delivery system for the
treatment of liver cancer:preclinical assessment in a rabbit
model of liver cancer. Clin Cancer Res 2006; 12 (8):2563–2567.
12. Constantin M, Fundueanu G, Bortolotti F, etal. Preparation
and characterisation of poly(vinyl alcohol)/cyclodextrin
microspheres as matrix for inclusion and separation of drugs.
Int J Pharm 2004; 285 (1–2):87–96.
13. Gonzalez MV, Tang Y, Phillips GJ, etal. Doxorubicin eluting
beads-2:methods for evaluating drug elution and in-vitro:in-vivo
correlation. J Mater Sci Mater Med 2008; 19 (2):767–775.
14. Lewis AL, Gonzalez MV, Leppard SW, etal. Doxorubicin eluting
beads– 1:eects of drug loading on bead characteristics and drug
distribution. J Mater Sci Mater Med 2007; 18 (9):1691–1699.
15. Lencioni R, de Baere T, Burrel M, etal. Transcatheter treatment
of hepatocellular carcinoma with doxorubicin-loaded DC bead
(DEBDOX):technical recommendations. Cardiovasc Intervent
Radiol 2012; 35 (5):980–985.
16. De Luis E, Bilbao JI, de Ciercoles JA, etal. In vivo evaluation of a
new embolic spherical particle (HepaSphere) in a kidney animal
model. Cardiovasc Intervent Radiol 2008; 31 (2):367–376.
17. Groupe d’Etude et de Traitement du Carcinome
Hepatocellulaire. A comparison of Lipiodol chemoembolization
and conservative treatment for unresectable hepatocellular
carcinoma. N Engl J Med 1995; 332 (19):1256–1261.
18. Lo CM, Ngan H, Tso WK, Liu CL, Lam CM, Poon RT,
etal. Randomized controlled trial of transarterial Lipiodol
chemoembolization for unresectable hepatocellular carcinoma.
Hepatology 2002; 35 (5):1164–1171.
19. Llovet JM, Real MI, Montana X, Planas R, Coll S, Aponte
J, etal. Arterial embolisation or chemoembolisation versus
symptomatic treatment in patients with unresectable
hepatocellular carcinoma:a randomised controlled trial. Lancet
2002; 359 (9319):1734–1739.
20. Aoki T, Imamura H, Hasegawa K, Matsukura A, Sano K,
Sugawara Y, etal. Sequential preoperative arterial and portal
venous embolizations in patients with hepatocellular carcinoma.
Arch Surg 2004; 139 (7):766–774.
21. Llovet JM, Burroughs A, Bruix J. Hepatocellular carcinoma.
Lancet 2003; 362 (9399):1907–1917.
22. Llovet JM. Treatment of hepatocellular carcinoma. Curr Treat
Options Gastroenterol 2004; 7 (6):431–441.
23. Arii S, Yamaoka Y, Futagawa S, Inoue K, Kobayashi K, Kojiro
M, etal. Results of surgical and nonsurgical treatment for
small-sized hepatocellular carcinomas:a retrospective and
nationwide survey in Japan. e Liver Cancer Study Group of
Japan. Hepatology 2000; 32 (6):1224–1229.
24. Livraghi T, Meloni F, Morabito A, Vettori C. Multimodal
image-guided tailored therapy of early and intermediate
hepatocellular carcinoma:long-term survival in the experience
of a single radiologic referral center. Liver Transpl 2004; 10 (2
Suppl 1):S98–S106.
25. Burger I, Hong K, Schulick R, Georgiades C, uluvath
P, Choti M, etal. Transcatheter arterial chemoembolization
in unresectable cholangiocarcinoma:initial experience
in a single institution. J Vasc Interv Radiol 2005; 16
(3):353–361.
26. Liapi E, Geschwind JF, Vossen JA, Buijs M, Georgiades CS,
Bluemke DA, etal. Functional MRI evaluation of tumor
response in patients with neuroendocrine hepatic metastasis
treated with transcatheter arterial chemoembolization. AJR Am
J Roentgenol 2008; 190 (1):67–73.
27. Sullivan KL. Hepatic artery chemoembolization. Semin Oncol
2002; 29 (2):145–151.
28. Vogl TJ, Zangos S, Eichler K, Yakoub D, Nabil M. Colorectal
liver metastases:regional chemotherapy via transarterial
chemoembolization (TACE) and hepatic chemoperfusion:an
update. Eur Radiol 2007; 17 (4):1025–1034.
29. De Baere T, Deschamps F, Teriitheau C, etal. Transarterial
chemoembolization of liver metastases from well
dierentiated gastroenteropancreatic endocrine tumors with
doxorubicin-eluting beads:preliminary results. J Vasc Interv
Radiol 2008; 19:855–861.
30. Forner A, Ayuso C, Varela M, etal. Evaluation of tumor response
aer locoregional therapies in hepatocellular carcinoma: are
response evaluation criteria in solid tumors reliable? Cancer
2009; 115:616–623.
31. Forner A, Llovet JM, Bruix J. Hepatocellular carcinoma. Lancet
2012; 379 (9822):1245–1255.
32. Georgiades CS, Liapi E, Frangakis C, etal. Prognostic
accuracy of 12 liver staging systems in patients with
unresectable hepatocellular carcinoma treated with
transarterial chemoembolization. J Vasc Interv Radiol 2006; 17
(10):1619–1624.
33. Liapi E, Hong K, Georgiades CS, Geschwind JF.
ree-dimensional rotational angiography:introduction of an
adjunctive tool for successful transarterial chemoembolization.
J Vasc Interv Radiol 2005; 16 (9):1241–1245.
34. Lencioni R, Llovet JM. Modied RECIST (mRECIST)
assessment for hepatocellular carcinoma. Semin Liver Dis 2010;
30:52–60.
35. Lim HK, Han JK. Hepatocellular carcinoma:evaluation of
therapeutic response to interventional procedures. Abdom
Imaging 2002; 27:168–179.
126
Chapter13:Chemoembolization technique and future potential
http://internalmedicinebook.com
36. Lin M, Pellerin O, Bhagat N, etal. Quantitative and volumetric
EASL and RECIST:feasibility of a semi-automated soware
method to assess tumor response aer transcatheter arterial
chemoembolization (TACE). J Vasc Intervent Radiol 2012; 23
(12):1629–1637.
37. Chapiro J, Wood LD, Lin M, Duran R, Geschwind JF, etal.
Radiologic–pathologic analysis of contrast-enhanced and
diusion-weighted MR imaging in patients with HCC aer
TACE:diagnostic accuracy of 3D quantitative image analysis.
Radiology 2014; Jul 15:140033.
38. Duran R, Chapiro J, Frangakis C, Lin M, Geschwind JF, etal.
Uveal melanoma metastatic to the liver:the role of quantitative
volumetric contrast-enhanced MR imaging in the assessment
of early tumor response aer transarterial chemoembolization.
Transl Oncol 2014; S1936–5233 (14):00059-X.
39. Fleckenstein FN, Schernthaner RE, Duran R, etal. 3D
Quantitative tumour burden analysis in patients with
hepatocellular carcinoma before TACE:comparing single-lesion
vs. multi-lesion imaging biomarkers as predictors of patient
survival. Eur Radiol 2016; 10.1007/s00330-015-4168-3.
40. Brown DB, Nikolic B, Covey AM, etal. Quality improvement
guidelines for transhepatic arterial chemoembolization,
embolization, and chemotherapeutic infusion for hepatic
malignancy. J Vasc Interv Radiol 2012; 23 (3):287–294.
41. Bouvier A, Ozenne V, Aube C, etal. Transarterial
chemoembolisation:eect of selectivity on tolerance, tumour
response and survival. Eur Radiol 2011; 21 (8):1719–1726.
42. Lammer J, Malagari K, Vogl T, etal. Prospective randomized
study of doxorubicin-eluting-bead embolization in the treatment
of hepatocellular carcinoma:results of the PRECISION V study.
Cardiovasc Intervent Radiol 2010; 33 (1):41–52.
43. Van Malenstein H, Maleux G, Vandecaveye V, etal. A
randomized phase II study of drug-eluting beads versus
transarterial chemoembolization for unresectable hepatocellular
carcinoma. Onkologie 2011; 34 (7):368–376.
44. Simonetti RG, Liberati A, Angiolini C, Pagliaro L. Treatment of
hepatocellular carcinoma:a systematic review of randomized
controlled trials. Ann Oncol 1997; 8 (2):117–136.
45. Gupta S, Johnson MM, Murthy R, Yao JC. Hepatic arterial
embolization and chemoembolization for the treatment of
patients with metastatic neuroendocrine tumors. Cancer 2005;
104 (8):1590–1602.
46. Reyes DK, Vossen JA, Kamel IR, etal. Single-center phase II
trial of transarterial chemoembolization with drug-eluting
beads for patients with unresectable hepatocellular
carcinoma:initial experience in the United States. Cancer J
2009; 15 (6):526–532.
47. Sergio A, Cristofori C, Cardin R, etal. Transcatheter arterial
chemoembolization (TACE) in hepatocellular carcinoma
(HCC):the role of angiogenesis and invasiveness. Am J
Gastroenterol 2008; 103 (4):914–921.
48. Scartozzi M, Faloppi L, Bianconi M, etal. e role of LDH
serum levels in predicting global outcome in HCC patients
undergoing TACE:implications for clinical management. PLoS
ONE 2012; 7 (3):e32653.
49. Llovet JM, Ricci S, Mazzaferro V, etal. Sorafenib in advanced
hepatocellular carcinoma. N Engl J Med 2008; 359 (4):378–390.
50. Pawlik TM, Reyes DK, Cosgrove D, Kamel IR, Bhagat N,
Geschwind JF. Phase II trial of sorafenib combined with
concurrent transarterial chemoembolization with drug-eluting
beads for hepatocellular carcinoma. J Clin Oncol 2011; 29
(30):3960–3967.
51. Geschwind JF, Kudo M, Marrero JA, etal. TACE treatment in
patients with sorafenib-treated unresectable hepatocellular
carcinoma in clinical practice:nal analysis of GIDEON.
Radiology 2016; 10.1148/radiol.2015150667:150667.
52. Bonekamp S, Li Z, Geschwind JF, etal. Unresectable
hepatocellular carcinoma:MR imaging after intraarterial
therapy. Part I.Identification and validation of volumetric
functional response criteria. Radiology 2013; 268
(2):420–430.
53. Loffroy R, Lin M, Yenokyan G, etal. Intraprocedural
C-arm dual-phase cone-beam CT:can it be used to predict
short-term response to TACE with drug-eluting beads in
patients with hepatocellular carcinoma? Radiology 2013; 266
(2):636–648.
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90
Yttrium radioembolization for hepatocellular
carcinoma
14
Ryan M. Hickey, Riad Salem, and Robert J. Lewandowski
Radioembolization refers to the intra-arterial, transcatheter
administration of micrometer-sized particles loaded with a
radioisotope, most commonly yttrium-90 (Y90). Because
liver tumors derive the majority of their blood supply from
hepatic arteries, as opposed to the predominantly portal
venous blood supply of normal liver tissue, hepatic arterial
injection of Y90-labeled microspheres results in greater deposition of the spheres in tumor tissue as opposed to normal
liver parenchyma.
1,2
Since Y90 radioembolization provides an
internal source of radiation to hepatic tumors, it is considered
brachytherapy.
Preferential deposition of radioactive microspheres within
tumor tissue provides for relative sparing of the uninvolved
liver parenchyma from the radiation eects of Y90, thereby
permitting signicantly higher radiation doses than can be
safely administered using external-beam radiation. e radiosensitive nature of normal liver tissue has traditionally limited
the role of external-beam radiation in the treatment of primary
and metastatic hepatic malignancies, as the incidence of severe
radiation-induced liver disease (RILD) may exceed 50% for
external-beam radiation doses greater than 35–40Gy. However,
with radioembolization, radiation doses in excess of 150Gy can
be safely administered.
3–6
Y90, a pure beta emitter with a half-life of 64.2hours and
tissue penetration of 2.5–11 mm, is incorporated into glass
or resin microspheres ranging in size from 20–30μm (glass)
to 20–60 μm (resin). Glass microspheres (erasphere, BTG
International Canada, Ottawa, ON, Canada) were approved in
1999 by the US Food and Drug Administration (FDA) under
a Humanitarian Device Exemption for the treatment of unresectable hepatocellular carcinoma (HCC).7 Resin microspheres
(SIR-Spheres, Sirtex Medical, Lane Cove, Australia) were
granted full premarketing approval in 2002 by the US FDA for
the treatment of unresectable colorectal metastases in conjunction with intrahepatic oxuridine.
8
Safe and eective treatment of hepatic tumors with radioembolization requires not only the angiographic and endovascular skills critical for selective embolization procedures,
but also a comprehensive understanding of radiation administration and safety, including radiation dosimetry and radiation dose modication based on tumor characteristics and a
patient’s clinical prole.
Patient selection
e patient selection process for Y90 radioembolization
involves an assessment of the patient’s burden of disease,
hepatic biochemical prole, and performance status. Patients
should have no extrahepatic disease and a tumor burden less
than 70% of the liver volume.
Hepatic reserve must be sucient to tolerate the eects of
radiation, typically indicated by bilirubin of ≤ 2 mg/dL and
albumin >3g/dL. Prothrombin time, a sensitive indicator of
hepatic synthetic function, should correspond to a normal
international normalized ratio (INR). Cancer-related symptoms
should be minimal, corresponding to an Eastern Cooperative
Oncology Group (ECOG) performance status of0–2.
Although the presence of portal vein thrombosis has been
traditionally considered a contraindication to hepatic arterial
embolization procedures, radioembolization has been shown
to be safe and eective in the setting of partial and branch
portal vein thrombosis.
9,10
Patients with prior interventions
involving the ampulla of Vater, including sphincterotomies,
hepaticoenteric anastomoses, or transampullary stents, are at
risk of developing hepatic abscesses following radioembolization and should be treated with caution. Aggressive antibiotic
coverage should be administered at the time of the procedure
and continued into the postprocedural period.
Technique
Y90 radioembolization involves two separate angiography
procedures – the mapping angiography and the treatment
angiography – both of which occur on an outpatient basis.
Radioembolization requires meticulous visceral and hepatic
angiography not only to establish the arterial supply to planned
treatment volumes necessary for radiation dosimetry, but also
in order to avoid the severe and detrimental adverse eects of
non-target, extrahepatic radioembolization.
An initial mapping angiography denes the hepatic arterial
anatomy supplying the planned treatment site, including variant
and/or accessory hepatic arterial pathways, as well as providing
the opportunity to identify and exclude extrahepatic perfusion
from the planned treatment site. Common variants of hepatic
arterial anatomy have been described11 and can signicantly
alter treatment planning and radiation dosimetry. Careful
Interventional Oncology, Second Edition, ed. Jean-François H. Geschwind and Michael C.Soulen. Published by Cambridge University Press.
©Cambridge University Press2016
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