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Chapter27:Prostate ablations
39. Humphrey PA. Complete histologic serial sectioning of a
prostate gland with adenocarcinoma. Am J Surg Pathol 1993; 17
(5):468–472.
40. Karavitakis M, Ahmed HU, Abel PD, Hazell S, Winkler MH.
Anatomically versus biologically unifocal prostate cancer:a
pathological evaluation in the context of focal therapy. er Adv
Urol 2012; 4 (4):155–160.
41. Ward JF, Jones JS. Focal cryotherapy for localized prostate
cancer:a report from the national Cryo On-Line Database
(COLD) Registry. BJU Int 2012; 109 (11):1648–1654.
42. Bott SRJ, Ahmed HU, Hindley RG, Abdul-Rahman A, Freeman
A, Emberton M. e index lesion and focal therapy:an analysis
of the pathological characteristics of prostate cancer. BJU Int
2010; 106 (11):1607–1611.
43. Mazzucchelli R, Scarpelli M, Cheng L, Lopez-Beltran A,
Galosi AB, Kirkali Z, etal. Pathology of prostate cancer and
focal therapy (‘male lumpectomy’). Anticancer Res 2009; 29
(12):5155–5161.
44. Stamey TA, Freiha FS, McNeal JE, Redwine EA, Whittemore AS,
Schmid HP. Localized prostate cancer. Relationship of tumor
volume to clinical signicance for treatment of prostate cancer.
Cancer 1993; 71 (3 Suppl):933–938.
45. Epstein JI, Walsh PC, Carmichael M, Brendler CB. Pathologic
and clinical ndings to predict tumor extent of nonpalpable
(stage T1c) prostate cancer. JAMA 1994; 271 (5):368–374.
46. Algaba F, Montironi R. Impact of prostate cancer multifocality
on its biology and treatment. J Endourol 2010; 24 (5):799–804.
47. Ahmed HU. e index lesion and the origin of prostate cancer.
N Engl J Med 2009; 361 (17):1704–1706.
48. Lin D, Bayani J, Wang Y, Sadar MD, Yoshimoto M, Gout PW,
etal. Development of metastatic and non-metastatic tumor
lines from a patient’s prostate cancer specimen-identication of
a small subpopulation with metastatic potential in the primary
tumor. Prostate 2010; 70 (15):1636–1644.
49. Wise AM, Stamey TA, McNeal JE, Clayton JL. Morphologic and
clinical signicance of multifocal prostate cancers in radical
prostatectomy specimens. Urology 2002; 60 (2):264–269.
50. Wolters T, Roobol MJ, van Leeuwen PJ, van den Bergh RCN,
Hoedemaeker RF, van Leenders GJLH, etal. A critical analysis
of the tumor volume threshold for clinically insignicant
prostate cancer using a data set of a randomized screening trial.
J Urol 2011; 185 (1):121–125.
51. Grasso CS, Wu Y-M, Robinson DR, Cao X, Dhanasekaran
SM, Khan AP, etal. e mutational landscape of lethal
castration-resistant prostate cancer. Nature 2012; 487
(7406):239–243.
52. Ganz PA, Barry JM, Burke W, Col NF, Corso PS, Dodson E,
etal. NIH State-of-the-Science Conference Statement:Role of
active surveillance in the management of men with localized
prostate cancer. NIH Consens State Sci Statements 2011; 28
(1):1–27.
53. Piersanti M, Ezzat S, Asa SL. Controversies in papillary
microcarcinoma of the thyroid. Endocr Pathol 2003; 14
(3):183–191.
54. Allegra CJ, Aberle DR, Ganschow P, Hahn SM, Lee CN,
Millon-Underwood S, etal. National Institutes of Health
State-of-the-Science Conference statement:diagnosis and
management of ductal carcinoma in situ September 22–24,
2009. J Natl Cancer Inst 2010; 102 (3):161–169.
55. Graversen JA, Mues AC, Perez-Lanzac de Lorca A, Landman J.
Active surveillance of renal cortical neoplasms:a contemporary
review. Postgrad Med 2011; 123 (1):105–113.
56. Kasivisvanathan V, Emberton M, Ahmed HU. Focal therapy
for prostate cancer:rationale and treatment opportunities. Clin
Oncol (R Coll Radiol) 2013; 25 (8):461–473.
57. Nevoux P, Ouzzane A, Ahmed HU, Emberton M, Montironi R,
Presti JC, etal. Quantitative tissue analyses of prostate cancer
foci in an unselected cystoprostatectomy series. BJU Int 2012;
110 (4):517–523.
58. Catto JWF, Robinson MC, Albertsen PC, Goepel JR, Abbod MF,
Linkens DA, etal. Suitability of PSA-detected localised prostate
cancers for focal therapy:experience from the ProtecT study. Br
J Cancer 2011; 105 (7):931–937.
59. Mouraviev V, Villers A, Bostwick DG, Wheeler TM, Montironi
R, Polascik TJ. Understanding the pathological features of
focality, grade and tumour volume of early-stage prostate
cancer as a foundation for parenchyma-sparing prostate cancer
therapies:active surveillance and focal targeted therapy. BJU Int
2011; 108 (7):1074–1085.
60. Masterson TA, Cheng L, Koch MO. Pathological
characterization of unifocal prostate cancers in whole-mount
radical prostatectomy specimens. BJU Int 2011; 107
(10):1587–1591.
61. Polascik TJ, Mayes JM, Schroeck FR, Sun L, Madden JF, Moul
JW, etal. Patient selection for hemiablative focal therapy of
prostate cancer:variables predictive of tumor unilaterality
based upon radical prostatectomy. Cancer 2009; 115
(10):2104–2110.
62. Montorsi F, Wilson TG, Rosen RC, Ahlering TE, Artibani
W, Carroll PR, etal. Best practices in robot-assisted radical
prostatectomy:recommendations of the Pasadena Consensus
Panel. Eur Urol 2012; 62 (3):368–381.
63. Eisenberg ML, Shinohara K. Partial salvage cryoablation of the
prostate for recurrent prostate cancer aer radiotherapy failure.
Urology 2008; 72 (6):1315–1318.
64. Pucar D, Shukla-Dave A, Hricak H, Moskowitz CS, Kuroiwa
K, Olgac S, etal. Prostate cancer:correlation of MR imaging
and MR spectroscopy with pathologic findings after
radiation therapy–initial experience. Radiology 2005; 236
(2):545–553.
65. Cellini N, Morganti AG, Mattiucci GC, Valentini V, Leone M,
Luzi S, etal. Analysis of intraprostatic failures in patients treated
with hormonal therapy and radiotherapy:implications for
conformal therapy planning. Int J Radiat Oncol Biol Phys 2002;
53 (3):595–599.
66. Arrayeh E, Westphalen AC, Kurhanewicz J, Roach M, Jung AJ,
Carroll PR, etal. Does local recurrence of prostate cancer aer
radiation therapy occur at the site of primary tumor? Results of
a longitudinal MRI and MRSI study. Int J Radiat Oncol Biol Phys
2012; 82 (5):787–793.
67. Rouviere O, Lyonnet D, Raudrant A, Colin-Pangaud C,
Chapelon JY, Bouvier R, etal. MRI appearance of prostate
following transrectal HIFU ablation of localized cancer. Eur Urol
2001; 40 (3):265–274.
68. Rouviere O, Glas L, Girouin N, Mege-Lechevallier F, Gelet
A, Dantony E, etal. Prostate cancer ablation with transrectal
high-intensity focused ultrasound:assessment of tissue
destruction with contrast-enhanced US. Radiology 2011; 259
(2):583–591.
279
Section IX:Prostate
69. Rouviere O, Girouin N, Glas L, Ben Cheikh A, Gelet A,
Mege-Lechevallier F, etal. Prostate cancer transrectal HIFU
ablation:detection of local recurrences using T2-weighted and
dynamic contrast-enhanced MRI. Eur Radiol 2010; 20 (1):48–55.
70. Fischer T, omas A, Tardy I, Schneider M, Hunigen H,
Custodis P, etal. Vascular endothelial growth factor receptor
2-specic microbubbles for molecular ultrasound detection
of prostate cancer in a rat model. Investig Radiol 2010; 45
(20733504):675–684.
71. Pochon S, Tardy I, Bussat P, Bettinger T, Brochot J, von
Wronski M, etal. BR55:a lipopeptide-based VEGFR2-targeted
ultrasound contrast agent for molecular imaging of
angiogenesis. Invest Radiol 2010; 45 (20027118):89–95.
72. Eggener S, Salomon G, Scardino PT, De la Rosette J, Polascik TJ,
Brewster S. Focal therapy for prostate cancer:possibilities and
limitations. Eur Urol 2010; 58 (20378241):57–64.
73. Gangi A, Tsoumakidou G, Abdelli O, Buy X, de Mathelin
M, Jacqmin D, etal. Percutaneous MR-guided cryoablation
of prostate cancer:initial experience. Eur Radiol 2012; 22
(8):1829–1835. PubMed PMID:22752525.
74. Cornelis F, Grenier N, Moonen CT, Quesson B. In vivo
characterization of tissue thermal properties of the
kidney during local hyperthermia induced by MR-guided
high-intensity focused ultrasound. NMR Biomed 2011; 24
(7):799–806. PubMed PMID:21834004.
75. Bomers JG, Yakar D, Overduin CG, Sedelaar JP, Vergunst H,
Barentsz JO, etal. MR imaging-guided focal cryoablation in
patients with recurrent prostate cancer. Radiology 2013; 268
(2):451–460. PubMed PMID:23525206.
76. Cornelis F, Havez M, Le Bras Y, Descat E, Richaud P, Grenier
N. Salvage CT-guided transgluteal cryoablation for locally
recurrent prostate cancer:initial experiences. J Vasc Interv
Radiol 2013; 24 (5):685–689. PubMed PMID:23622040.
77. Ryan ER, Sofocleous CT, Schoder H, Carrasquillo JA, Nehmeh
S, Larson SM, etal. Split-dose technique for FDG PET/
CT-guided percutaneous ablation:a method to facilitate lesion
targeting and to provide immediate assessment of treatment
eectiveness. Radiology 2013; 268 (1):288–295. PubMed
PMID:23564714. Pubmed Central PMCID:3689447.
78. Detti B, Scoccianti S, Franceschini D, Cipressi S, Cassani S,
Villari D, etal. Predictive factors of [18F]-choline PET/CT
in 170 patients with increasing PSA aer primary radical
treatment. J Cancer Res Clin Oncol 2013; 139 (3):521–528.
PubMed PMID:23183655.
79. Bundschuh RA, Wendl CM, Weirich G, Eiber M, Souvatzoglou
M, Treiber U, etal. Tumour volume delineation in prostate
cancer assessed by [11C]choline PET/CT:validation with
surgical specimens. Eur J Nucl Med Mol Imaging 2013; 40
(6):824–831. PubMed PMID:23389430.
80. Sapareto SA, Dewey WC. ermal dose determination in cancer
therapy. Int J Radiat Oncol Biol Phys 1984; 10 (6):787–800.
PubMed PMID:6547421. Epub 1984/06/01.eng.
81. Susani M, Madersbacher S, Kratzik C, Vingers L, Marberger
M. Morphology of tissue destruction induced by focused
ultrasound. Eur Urol 1993; 23 Suppl 1:34–38. PubMed
PMID:8513832.
82. Crouzet SM, Kirchner H, orpe SJ. Fast saccades toward
faces:face detection in just 100 ms. J Vision 2010; 10 (4):1–7.
PubMed PMID:20465335.
83. Stride EP, Coussios CC. Cavitation and contrast:the use of
bubbles in ultrasound imaging and therapy. Proceedings of the
Institution of Mechanical Engineers Part H. J Eng Med 2010; 224
(2):171–191. PubMed PMID:20349814.
84. Muto S, Yoshii T, Saito K, Kamiyama Y, Ide H, Horie S.
Focal therapy with high-intensity-focused ultrasound in the
treatment of localized prostate cancer. Jpn J Clin Oncol 2008; 38
(3):192–199.
85. Bahn DK, Silverman P, Lee F, Badalament R, Bahn ED,
Rewcastle JC. Focal prostate cryoablation:initial results show
cancer control and potency preservation. J Endourol 2006; 20
(16999628):688–692.
86. Gonder MJ, Soanes WA, Shulman S. Cryosurgical treatment
of the prostate. Invest Urol 1966; 3 (4):372–378. PubMed
PMID:4160242. Epub 1966/01/01.eng.
87. Onik G, Vaughan D, Lotenfoe R, Dineen M, Brady J. e
“male lumpectomy”:focal therapy for prostate cancer using
cryoablation results in 48 patients with at least 2-year follow-up.
Urol Oncol 2008; 26 (18774463):500–505.
88. El Hayek OR, Alfer W, Jr., Reggio E, Pompeo AC, Arap
S, Srougi M. Percutaneous prostate cryoablation as
treatment for high-risk prostate cancer. Clinics (Sao Paulo)
2007; 62 (2):109–112. PubMed PMID:17505693. Epub
2007/05/17.eng.
89. Mouraviev V, Spiess PE, Jones JS. Salvage cryoablation
for locally recurrent prostate cancer following primary
radiotherapy. EurUrol 2012; 61 (6):1204–1211. PubMed
PMID:22421081. Epub 2012/03/17.eng.
90. Erinjeri JP, Clark TW. Cryoablation:mechanism of action
and devices. J Vasc Interv Radiol 2010; 21 (8 Suppl):S187–S91.
PubMed PMID:20656228.
91. Wang J, Sefah K, Altman MB, Chen T, You M, Zhao Z, etal.
Aptamer-conjugated nanorods for targeted photothermal
therapy of prostate cancer stem cells. Chemistry 2013; 8
(10):2417–2422. PubMed PMID:23757285.
92. Gobin AM, Moon JJ, West JL. EphrinA I-targeted nanoshells
for photothermal ablation of prostate cancer cells. Int J
Nanomedicine 2008; 3 (3):351–358. PubMed PMID:18990944.
Pubmed Central PMCID:2626934.
93. Chen YY, Hossack T, Woo H. Long-term results of bipolar
radiofrequency needle ablation of the prostate for lower urinary
tract symptoms. J Endourol 2011; 25 (5):837–840. PubMed
PMID:21476862.
94. Jindal G, Friedman M, Locklin J, Wood BJ. Palliative
radiofrequency ablation for recurrent prostate cancer.
Cardiovasc Interv Radiol 2006; 29 (3):482–485. PubMed
PMID:16010507. Pubmed Central PMCID:2386884.
95. Onik G, Mikus P, Rubinsky B. Irreversible electroporation:
implications for prostate ablation. Technol Cancer Res Treat 2007;
6 (4):295–300. PubMed PMID:17668936.
96. Bower M, Sherwood L, Li Y, Martin R. Irreversible
electroporation of the pancreas:denitive local therapy without
systemic eects. J Surg Oncol 2011; 104 (1):22–28. PubMed
PMID:21360714.
97. Tian Y, Leung W, Yue K, Mak N. Cell death induced by
MPPa-PDT in prostate carcinoma in vitro and in vivo.
Biochem Biophys Res Commun 2006; 348 (2):413–420. PubMed
PMID:16889752.
98. Liang X, Wang KK, Zhu TC. Feasibility of interstitial diuse
optical tomography using cylindrical diusing bers for
prostate PDT. Phys Med Biol 2013; 58 (10):3461–3480. PubMed
PMID:23629149. Pubmed Central PMCID:3759155.
280
Chapter27:Prostate ablations
99. Song DY, DeWeese TL. Can PSA nadir predict prostate cancer
outcomes following radiotherapy? Nat Clin Pract Urol 2006; 3
(9):464–465. PubMed PMID:16964182.
100. Crouzet S, Chapelon JY, Rouviere O, Mege-Lechevallier
F, Colombel M, Tonoli-Catez H, etal. Whole-gland
ablation of localized prostate cancer with high-intensity
focused ultrasound:oncologic outcomes and morbidity
in 1002 patients. Eur Urol 2014; 65 (5): 907–914. PubMed
PMID:23669165.
101. Roach M, Hanks G, ames H, Schellhammer P, Shipley
WU, Sokol GH, etal. Dening biochemical failure following
radiotherapy with or without hormonal therapy in men with
clinically localized prostate cancer:recommendations of the
RTOG-ASTRO Phoenix Consensus Conference. Int J Radiat
Oncol Biol Phys 2006; 65 (4):965–974.
102. Ganzer R, Robertson CN, Ward JF, Brown SCW, Conti GN,
Murat FJ, etal. Correlation of prostate-specic antigen nadir
and biochemical failure aer high-intensity focused ultrasound
of localized prostate cancer based on the Stuttgart failure
criteria– analysis from the @-Registry. BJU Int 2011; 108
(8):196–201.
103. Nguyen PL, Chen M-H, D’Amico AV, Tempany CM, Steele
GS, Albert M, etal. Magnetic resonance image-guided salvage
brachytherapy aer radiation in select men who initially
presented with favorable-risk prostate cancer:a prospective
phase 2 study. Cancer 2007; 110 (7):1485–1492.
104. Goldberg SN, Grassi CJ, Cardella JF, Charboneau JW,
Dodd GD, 3rd, Dupuy DE, etal. Image-guided tumor
ablation:standardization of terminology and reporting criteria.
J Vasc Interv Radiol JVIR. 2009; 20 (7 Suppl):S377–S390.
PubMed PMID:19560026.
105. Robertson NL, Moore CM, Ambler G, Bott SR, Freeman
A, Gambarota G, etal. MAPPED study design:a 6month
randomised controlled study to evaluate the eect of
dutasteride on prostate cancer volume using magnetic
resonance imaging. Contemp Clin Trials 2013; 34 (1):80–89.
PubMed PMID:23085153.
106. Barret E, Ahallal Y, Sanchez-Salas R, Galiano M, Cosset J-M,
Validire P, etal. Morbidity of focal therapy in the treatment of
localized prostate cancer. Eur Urol 2013; 63 (4):618–622.
107. Lindner U, Trachtenberg J, Lawrentschuk N. Focal therapy in
prostate cancer:modalities, ndings and future considerations.
Nat Rev Urol 2010; 7 (10):562–571.
108. El Fegoun AB, Barret E, Prapotnich D, Soon S, Cathelineau
X, Rozet F, etal. Focal therapy with high-intensity focused
ultrasound for prostate cancer in the elderly. Afeasibility study
with 10years follow-up. Int Braz J Urol 2011; 37 (2):213–219.
109. Ahmed HU, Freeman A, Kirkham A, Sahu M, Scott R, Allen
110. Rabbani F, Yunis LH, Pinochet R, Nogueira L, Vora KC,
Eastham JA, etal. Comprehensive standardized report
of complications of retropubic and laparoscopic radical
prostatectomy. Eur Urol 2010; 57 (3):371–386.
111. Shariat SF, Raptidis G, Masatoschi M, Bergamaschi F, Slawin
KM. Pilot study of radiofrequency interstitial tumor ablation
(RITA) for the treatment of radio-recurrent prostate cancer.
Prostate 2005; 65 (3):260–267.
112. Bahn D, de Castro Abreu AL, Gill IS, Hung AJ, Silverman P,
Gross ME, etal. Focal cryotherapy for clinically unilateral,
low-intermediate risk prostate cancer in 73 men with a median
follow-up of 3.7years. Eur Urol 2012; 62 (1):55–63.
113. Moore CM, Nathan TR, Lees WR, Mosse CA, Freeman A,
Emberton M, etal. Photodynamic therapy using meso tetra
hydroxy phenyl chlorin (mTHPC) in early prostate cancer.
Lasers Surg Med 2006; 38 (5):356–363.
114. Ganzer R, Fritsche HM, Brandtner A, Brundl J, Koch D,
Wieland WF, etal. Fourteen-year oncological and functional
outcomes of high-intensity focused ultrasound in localized
prostate cancer. BJU Int 2013; 112 (3):322–329. PubMed
PMID:23356910.
115. Inoue Y, Goto K, Hayashi T, Hayashi M. Transrectal
high-intensity focused ultrasound for treatment of localized
prostate cancer. Int J Urol 2011; 18 (5):358–362. PubMed
PMID:21449970.
116. Blana A, Rogenhofer S, Ganzer R, Lunz JC, Schostak M,
Wieland WF, etal. Eight years’ experience with high-intensity
focused ultrasonography for treatment of localized prostate
cancer. Urology 2008; 72 (6):1329–1333; discussion 33–34.
PubMed PMID:18829078.
117. Blana A, Murat FJ, Walter B, uro S, Wieland WF, Chaussy
C, etal. First analysis of the long-term results with transrectal
HIFU in patients with localised prostate cancer. Eur Urol 2008;
53 (6):1194–1201. PubMed PMID:17997026.
118. Cheetham P, Truesdale M, Chaudhury S, Wenske S, Hruby
GW, Katz A. Long-term cancer-specic and overall survival
for men followed more than 10years aer primary and
salvage cryoablation of the prostate. J Endourol 2010; 24
(7):1123–1129. PubMed PMID:20575687.
119. Onik G, Vaughan D, Lotenfoe R, Dineen M, Brady J. e
“male lumpectomy”:focal therapy for prostate cancer
using cryoablation results in 48 patients with at least 2-year
follow-up. Urol Oncol 2008; 26 (5):500–505.
120. Bahn DK, Lee F, Badalament R, Kumar A, Greski J, Chernick
M. Targeted cryoablation of the prostate:7-year outcomes in
the primary treatment of prostate cancer. Urology 2002; 60 (2
Suppl 1):3–11. PubMed PMID:12206842.
C, etal. Focal therapy for localized prostate cancer:a phase I/II
trial. J Urol 2011; 185 (4):1246–1254.
281
Section X
Chapter
Specialized interventional techniques in cancer care
Vascular access:Venous and arterialports
28
ierry de Baère and Eric Desruennes
Hepatic intra-arterialport
Indications
Because hepatic artery infusion chemotherapy (HAIC) is a
local treatment, it is most oen used in case of liver cancer
without extrahepatic disease, or in patients with predominant
hepatic disease.
1,2
Such treatment has been used mostly as salvage therapies aer failure of intravenous (IV) standard-ofcare therapies for metastases, and because response rate
remains interesting even when using the same drug that was
or became inecient with IV administration. Due to the high
response rate of HAIC, there are some recent reports and ongoing study using such therapies in rst line. e goal of such
therapies in rst line, as a so-called induction treatment, is to
obtain as early as possible in the disease the highest response
possible in order to downstage a non-surgical candidate to a
surgical candidate.2 Indeed, it has been demonstrated that the
increase in response rate of colorectal liver-only metastases
(CRLM) to treatment is linearly correlated with an increase
in resection rate, and consequently with an increased chance
of cure.3 Such induction chemotherapy targeting specically
the liver is obviously even more interesting in patients with
liver-limited disease which demonstrated a steeper slope of
the linear correlation between response and downstaging from
non-operable to surgical candidates. HAIC used in an adjuvant
setting aer liver resection has been demonstrated to increase
survival.
4
For primary tumors, and namely hepatocellular carcinoma,
the use of HAIC is less common due to the high ecacy of transarterial chemoembolization (TACE). Indications are probably
in patients not responding to TACE or not candidates for TACE
due to portal vein thrombosis or advanced liver insuciency.
HAIC is technically more challenging than systemic chemotherapy, because it requires the implantation of an indwelling
catheter in the hepatic artery that is connected to a subcutaneous port for the administration of repeated courses of HAIC.
e main drawbacks that hampered the use of HAIC were
that, until recently, the implantation of such a device required
a laparotomy, and additionally, frequent catheter dysfunction
led to discontinued treatment. For example, in a randomized
controlled study comparing HAIC with 5-uorouracil (5-FU)
to systemic 5-FU in 290 cases, 50 (37%) patients allocated to
HAIC did not start their treatment, and another 39 (29%) had
to stop before receiving six cycles of treatment because of catheter failure. Only 33% of patients received at least six courses
of HAIC vs. 78% for the IV route.7 e HAIC group received
a median of two cycles (0–6), compared to 8.5 (6–12) for the
IV group. Such problems could be reduced with the use of the
percutaneous technique for catheter implantation and revision.
Rationale
Colorectal cancer is the most frequent cancer in the Western
world, and the most common cause of death from this cancer is due to hepatic metastases. Hepatic metastases from
colorectal cancer will occur in 50–75% of patients during the
disease. Twenty percent are present at time of diagnosis and
30–50% will appear later. Even if surgery is the best treatment option for liver metastases, it will be possible in only
20% of patients, and furthermore 70% of patients who underwent surgery will develop new CRLM. Consequently, there is
a large place for chemotherapy in order to treat liver metastases. Despite the high response rate with modern regimens,
including 5-FU-oxaliplatin and 5-FU-irinotecan, there are still
non-responders who can benet from HAIC, which proved to
provide response in non-responders to the previously mentioned regimens.
Directly administering chemotherapy in the hepatic artery
oers three theoretical advantages for patients with unresectable tumors conned to the liver. Firstly, higher drug concentrations are delivered to the tumor compared with systemic
infusion. Secondly, HAIC capitalizes on the fact that liver vas-
5,6
cularization is 30% arterial and 70% portal. As liver tumors
are nearly exclusively nourished by arterial blood ow, the
drug injected into the hepatic artery will preferentially reach
the tumor. Finally, if the drug is eliminated by hepatic extraction, lower systemic concentrations and thus lower systemic
toxicities may be expected than aer systemic infusion. As
a consequence, HAIC has the main advantage of increasing drug concentrations in tumor deposits, thus resulting in
a signicant increase in response rates because many tumors
Interventional Oncology, Second Edition, ed. Jean-François H.Geschwind and Michael C.Soulen. Published by Cambridge University Press.
©Cambridge University Press2016
283
Section X:Specialized interventional techniques in cancercare
display a steep dose–response curve. e advantage for such
intra-arterial route is proportional to rst-pass extraction of
the drug by the liver and inversely proportional to body clearance of the drug. Consequently, the choice of drug is of utmost
importance. Floxuridine (FUDR) has been extensively used
for HAIC because it is extracted by the liver at more than 95%
during the rst pass, with an increase of exposure of the liver
100–300 times higher than with systemic perfusion. When
compared to IV perfusion, the estimated increase in liver
exposure by HAIC is about 20-fold for THP-Adriamycin (pirarubicin), ve–tenfold for 5-FU, four–sevenfold for cisplatin,
six–eightfold for mitomycin, fourfold for oxaliplatin, and only
twofold for doxorubicin.
All clinical trials using 5-FU or FUDR have demonstrated a
better response rate for HAIC than for IV treatments. However,
only few trials have demonstrated a benet in survival.
Intra-arterial chemotherapy was more or less abandoned at the
time IV irinotecan and oxaliplatin proved to give equivalent
response rate to intra-arterial 5-FU. However, recently a French
multicentric trial has used these new drugs intra-arterially,
with HAIC using 100mg/m2 of oxaliplatin repeated every second week, with overall response rate of 64% (95% condence
interval (CI), 44–81%) in heavily pretreated patients.10 In addition, new drug combinations including HAIC plus IV oxaliplatin and irinotecan allowed as high a rate as 88% of tumor
response.
11
Such treatment required injection scheduled every second
week and consequently it is not convenient to repeat peripheral arterial access and hepatic artery catheterization for each
subsequent course of chemotherapy. As a result, a permanent
and easy access route has to be obtained with port linked to
an intra-arterial catheter. In the past, implantation of ports
for intra-arterial hepatic chemotherapies required laparotomy. Recently, a laparoscopic approach has been reported in
a small series.12 In the past, the percutaneous approach has
been used to place the catheter in the hepatic artery for chemotherapy with the need for repeated peripheral arterial access
and hepatic artery catheterization for each subsequent chemotherapy delivery.13 Today minimally invasive techniques allow
placement of catheter/port systems for HAIC without the need
for open surgery or repeated catheterization.
manual compression of the axillary artery, which led some
teams to access the axillary artery through surgical exposure
and cutdown of the thoracic-acromial artery.15 Strokes are due
to emboli induced by the body of the catheter lying in front
of the origin of the le vertebral artery, and for some authors
retrieval or exchange of such catheter is risky enough to make
them recommend that such maneuvers should be performed
through a femoral access if possible.15 Using the femoral artery
for catheter port insertion is technically more challenging but
can be achieved nowadays in the vast majority of patients due
to improvement in endovascular material design. Furthermore,
femoral access will most oen be needed for endovascular ow
remodeling, even if the indwelling catheter is inserted through
the axillaryroute.
8,9
Arterial ow remodeling
Flow remodeling is nearly always needed before indwelling
catheter insertion, because HAIC needs to perfuse the entire
liver and only the liver through a single artery (Figure28.1).
First, replaced hepatic arteries should be occluded proximally
with stainless-steel coils, reproducing by endovascular techniques surgical ligation, in order to allow perfusion of the complete liver through a single catheter (Figure 28.2). Secondly,
arteries not feeding the liver, feeding the stomach, the duodenum, or the pancreas, which arise between the perfusion hole
in the catheter and liver, should be occluded to avoid toxicity of
extrahepatic drug perfusion. In clinical practice, the gastroduodenal artery and the right gastric artery are the more frequent
arteries requiring endovascular occlusion because it is rarely
possible to place the perfusion hole of the catheter downstream
of them. Occlusion of the right gastric artery is a key factor to
lower toxicity of infused drug to the liver, as discussed in the
results section.
Right gastric artery occlusion is probably the most technically challenging part of HAIC catheter insertion. Firstly, it is
sometimes dicult to see it on the hepatic artery angiogram;
secondly, it can arise anywhere between the common hepatic
artery and the distal part of the le branch of the hepatic
artery. When its origin cannot be seen on the hepatic artery
angiogram it is oen useful to perform selective angiogram
of the le gastric artery. In most instances retrograde injection in the right gastric artery will be seen and it will help to
Technique
Accessroute
e catheter is usually introduced through the axillary or femoral arteries.
only one series.17 e axillary route has been more described
14,15,16
e intercostal artery route was reported in
than the femoral route. It was preferred because it allows easier insertion of the catheter into the hepatic artery due to the
usually descending orientation of the initial part of the celiac
trunk, thus avoiding the sharp angulation encountered when
using femoral access. e disadvantages of the axillary route
are a higher rate of overall and severe complications, including up to 3% of aneurysms requiring arterial stent for treatment which induce axillary artery thrombosis,16 and 0.5–1%
of stroke.
13,15
Aneurysms are due to the diculty of access and
determine the location of the origin of the right gastric artery
from the hepatic artery (Figure28.3). Sometimes it will be
possible to perform hyperselective catheterization of the le
gastric and then retrograde catheterization of the right gastric to perform coil embolization of its origin (Figure28.3).
e absence of reported toxic eect on gallbladder makes it
unnecessary to systematically occlude vessels that feed the
gallbladder; however, a very large cystic artery should probably be occluded.
Catheter positioning
e HAIC catheter can be placed oating in the hepatic artery
lumen, with risk of migration. Stability of the catheter tip is
obtained by inserting the catheter deeply in the gastroduodenal artery or, when this is impossible, in a distal branch of the
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A B
Chapter28:Vascular access:Venous and arterialports
C
Figure 28.1 Schematic drawing of the three different techniques of catheter implantation. (A) Schematic drawing of steps needed for implantation of an
intra-arterial catheter with distal tip in the gastroduodenal artery. Normal anatomy (1), coil inserted in the right gastric artery (2), indwelling catheter in lace with
side hole in the distal part of the common hepatic artery (3), coils in the gastroduodenal artery around the catheter (4), and flow of chemotherapy through the
implanted catheter (5). (B) Schematic drawing of a free-floating catheter implanted in the hepatic artery proper after coil occlusion of the gastroduodenal and right
gastric arteries. (C) Schematic drawing of a catheter implanted distally in a peripheral branch of the hepatic artery after coil occlusion of the gastroduodenal and
right gastric arteries.
hepatic artery, and placing the side hole of the indwelling catheter in the hepatic artery upstream of its rst bifurcation. When
the catheter tip is in the gastroduodenal artery, coils and/or
cyanoacrylate glue are delivered around it, in order to provide
both xation of the catheter and occlusion of the gastroduodenal artery. e distal portion of the catheter lumen, between
the side hole and the distal hole, will spontaneously occlude in
a few minutes to a few hours due to clotting. In practice, aer
the initial angiogram and occlusion of the replaced hepatic
artery and right gastric artery, the gastroduodenal artery is
catheterized as distally as possible down to the distal right epiploic artery with a microcatheter (2.4–2.8F). en a sti 0.018
guidewire is placed for over-the-wire insertion of the infusion
catheter, with its distal tip inserted in the gastroduodenal artery.
e infusion catheter has a side hole located 7–10cm from the
tip and is tapered from 5 to 2.7F (ST-305C, B.Braun Medical,
Center Valley, USA). e side hole is le in the terminal part of
the common hepatic artery and will be used for chemotherapy
drug infusion. en, occlusion of the gastroduodenal artery
around the indwelling catheter can be obtained with a second
catheter introduced through contralateral femoral puncture.
More interestingly, a microcatheter can be inserted in the
indwelling catheter and throughout the side hole and passed
down to the gastroduodenal artery for occlusion with 0.018
coils. en, the proximal part of the indwelling catheter is tunneled and attached to a port placed on either the chest wall
or the pelvic wall according to access route. Catheter maintenance means ushing with heparin solution (500IU/10mL)
aer completion of chemotherapy until the next course.
Angiographic control or radionuclide control is performed
routinely, every two courses, to check patency and perfusion
territory of the catheter.
When catheterization of the GDA is not possible, a
free-oating catheter can be placed, with its distal tip pushed
far in the intrahepatic portion of the hepatic artery, and the
side hole will be placed in the hepatic artery 1–2cm upstream
of the rst bifurcation of the hepatic artery in right and le
branches.
Contraindications
e hepatic artery must be patent to allow for HAIC and occlusion or severe stenosis of the hepatic artery are contraindications.
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Section X:Specialized interventional techniques in cancercare
AB
DE
C
Figure 28.2 Angiograms during implantation of an intra-arterial hepatic catheter with distal tip in the gastroduodenal artery. (A) Angiogram obtained after
injection in the middle hepatic artery shows a branch for the left liver (arrow), and the gastroduodenal artery. The right gastric artery can be faintly seen
(arrowheads). (B) Angiogram obtained after injection in the superior mesenteric artery shows a replaced right hepatic artery. (C) After occlusion of the replaced
right hepatic artery with an endovascular occluding device (arrow), the contrast medium is seen in the proximal part of the replaced right hepatic artery
(arrowheads). (D) Distal part of the 5 French indwelling catheter demonstrating a side hole (arrow). By shortening the catheter, distance from the side hole to the
tip will be customized for each patient according to the anatomy. Usually the side hole is between 7 and 10 cm from the tip. (E) The right gastric artery has been
occluded with coils (black arrowheads) and the tip of the indwelling catheter (white arrow) has been placed in the gastroduodenal artery which has also been
occluded with coils (black arrows). Injection of contrast medium in the femoral-implanted port opacifies the complete hepatic vascularization and only hepatic
arteries through the side hole of the catheter. Note the collateral arterial pathways through the liver hilum that vascularized the right hepatic artery distal to the
occluding device (white arrowhead).
ABC
Figure 28.3 The reverse technique for occlusion of the right gastric artery. (A) Angiogram obtained after injection in the middle hepatic artery shows a usual
anatomy with right and left branches to the liver and gastroduodenal artery. The right gastric artery (arrow) can be faintly seen arising from the left branch of the
hepatic artery. This branch could not be catheterized through the left hepatic artery. (B) Injection in the left gastric artery demonstrates all the artery from the small
curvature of the stomach (arrows) and reverse opacification of the right gastric to the left branch of the hepatic artery (arrowhead). (C) A 0.018-inch guidewire has
been inserted from the celiac trunk, through the left gastric then the right gastric to reach the left branch of the hepatic artery and will allow coiling of the origin of
the right gastric.
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Chapter28:Vascular access:Venous and arterialports
In the same manner, retrograde ow due to severe stenosis of
the celiac trunk does not allow for port-catheter placement.
e artery chosen for access (femoral or axillary) must be patent and free of any stenosis or severe atherosclerotic disease,
in order to avoid thrombosis aer insertion of the indwelling
catheter. Because material will be implanted, in order to avoid
local sepsis, the patient must not have local or general sepsis
before catheter placement. Patency of the portal system is not
mandatory but one should be aware that, in cases with compromised portal vein patency, if the indwelling catheter induces
hepatic artery thrombosis there is a risk of hepatic necrosis.
Results
Port/catheter placement
Technical success of catheter insertion is very high and close
to 100% in most series.15 In our experience the initial success
rate of the femoral approach at a rst attempt was 92% (48/52),
and the overall success of the catheter implantation was 98%
(51/52), including three patients, with a second attempt
through the femoral artery in two and a subclavian artery in
one patient.18 Catheter infusion hole migration is signicantly
higher for a free-oating catheter (50%) vs. catheter tip in
the gastroduodenal artery (14%; P=0.032) or catheter tip in
a distal hepatic artery (0%; P=0.024), without any dierence
between the lasttwo.
18
A large series of percutaneous implantation reports patency
of 91%, 81%, and 58% at 6months, 1year, and 2years, allowing
3–102 courses of chemotherapy (mean=35).15 Astudy comparing percutaneously and surgically placed catheter/ports
reported an overall incidence of device-related complications
causing temporary or denitive suppression of HAIC in 42.7%
of percutaneous placements and 7.1% of surgical ones.19 But
rates of complication are the same if the 35.7% of tip migration in the percutaneous group are not taken into account.
Indeed, such migration would not have occurred if the catheter tips had been lodged in the gastroduodenal artery instead
of being free-oating in the hepatic artery. Hospital stay and
analgesic requirements were signicantly lower in the percutaneous group (1.8±0.7days and 2±0.9 doses respectively)
than in the surgical group (8.2±22days and 9.7±3.2 doses).
Interestingly, gastroduodenal complications related to chemotherapy toxicity in cases of extrahepatic perfusion were lower
in the percutaneous group (7.1%) than in the surgical group
(17.8%).
19
In a comparative study, the success rates of implantation
were 97% (65/67) for percutaneous placement and 98% (58/59)
for surgical implantation.18 Among 107 patients, primary
functionality was not dierent for percutaneous placement
(n=4.80 courses) vs. surgical implantation (n=4.82 courses),
but functionality aer revision was signicantly higher for
percutaneous versus surgical placement (9.18 vs. 5.95 courses;
P=0.004). is increased secondary patency is due to easier
revision of percutaneous placed port versus surgical ones. e
rates of discontinuation of HAIC linked to complications of the
port-catheters were 21% for percutaneous and 34% for surgical
implantation.
18
e most common complication of HAIC is gastroduodenal ulceration due to perfusion of chemotherapy in an extrahepatic feeder that remains patent beyond the location of the
catheter tip. e main artery responsible for such complication
is the right gastric artery, which needs all possible eort to be
embolized. Indeed, gastroduodenal ulcerations are signicantly
lower (P=0.019) when the right gastric artery is embolized
than when it is not, 5%.18 e success rate of the right gastric
artery embolization signicantly improved, from 17% among
the 23 rst patients to 66% (n=16) among the 24 last ones
(P = 0.0006) due to the learning curve of the interventional
radiologist.18 Embolization of the cystic artery is not mandatory, because no cholecystitis has been reported in three series,
including altogether 153 patients with percutaneous implanted
catheter/ports, including only eight cholecystectomized patie
14,16,19
nts.
rombosis of the hepatic artery is rare, and seems to
be related to the size of the indwelling catheter, namely when a
catheter larger than 5F is placed in the hepatic artery. Infection
of the port and femoral artery thrombosis are reported in less
than2%.
Interventional radiologists have a role to play in malfunctions aecting surgically placed hepatic arterial ports with high
ecacy for restoring complete liver perfusion in case of anatomical variation or extrahepatic perfusion not seen at time of
surgery or in case of catheter thrombosis or hepatic arterial stenosis, dissection, or occlusion.20 On the other hand, interventional radiology and endovascular maneuvers are most oen
not ecient in thrombosis or dissection of the hepatic artery.
20
Chemotherapy
5-FU and systemic 5-uoro-2'-deoxyuridine (FUDR, a pyrimidine antimetabolite transformed to 5-FU in the liver) were
the rst two drugs used for HAIC. eir use was supported
by pharmacological results which demonstrated a hepatic
extraction ratio of 19–51% for 5-FU and 94–99% for FUDR.
is results in lower systemic drug levels aer HAIC than aer
systemic injection (60% for 5-FU and 25% for FUDR).21 Asignicant pharmacokinetic advantage was demonstrated with
oxaliplatin when administered via the intra-arterial route compared to systemic administration, with a 4.3-fold increase in
drug concentration in the tumor compared to that observed in
healthy hepatic tissue.
ese pharmacological advantages of HAIC have resulted
in a signicantly increased response rate. Seven randomized
studies compared HAIC with FUDR to intravenous 5-FU,
intravenous FUDR, or the best supportive care at a time when
IV 5-FU combined with folinic acid was the standard regimen
for CRLM. All these trials favored HAIC in terms of response
rates (42–62% versus 10–21% respectively), but only two trials demonstrated a survival benet with HAIC.
cooperative studies were subsequently performed but they
provided contradictory results.
nicantly improved survival (24.4 vs. 20months), but shorter
time to extrahepatic progression (7.7 vs 14.8months) for HAIC
compared to IV chemotherapy.
Modern regimens (combining systemic 5-FU with oxaliplatin, irinotecan, or both) yield similar response rates to
22
23,24
Two major
9,25
Kemeny etal.9 reported sig-
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Section X:Specialized interventional techniques in cancercare
those observed aer HAIC containing 5-FU or FUDR. Indeed,
the response rates reported with FOLFOX or FOLFIRI are
40–45% and as high as 66% with the FOLFOXIRI regimen, with overall survival of 17–20months with FOLFOX
or FOLFIRI and 23months with FOLFOXIRI. ese results
have challenged the benet gained using the intra-arterial
route, especially as HAIC alone is probably less ecient
against occult extrahepatic disease. Consequently, systemic
modern drugs (irinotecan, oxaliplatin, bevacizumab, cetuximab) were introduced in HAIC regimens either given as
an injection in the hepatic artery or in combination with
HAIC-FUDR. HAI oxaliplatin combined with IV 5-FU demonstrated that an overall response rate was 62% among the
39 assessable patients, including 17, 12, and 12 patients who
had failed to respond to prior systemic chemotherapy with
FOLFIRI, FOLFOX, or both, respectively.1 In this report, further R0 surgical resection can be proposed in 18% of initially
unresectable CRLM and radiofrequency ablation in 2%.
Atriple combination including HAIC with FUDR plus IV
oxaliplatin and irinotecan provided as high as 90% of tumor
response.
11
More recently, 49 patients with unresectable CRLM (53%
previously treated with chemotherapy) were enrolled on to
a phase Iprotocol with HAI oxuridine and dexamethasone
plus systemic chemotherapy with oxaliplatin and irinotecan.2
In this study, more than ve CRLM were present in 73% of
patients, 98% had bilobar disease, and 86% had six segments or
more involved. Ninety-two percent of the 49 patients had complete (8%) or partial (84%) response, and 47% (23/49) of the
patients were able to undergo resection in a group of patients
with extensive disease. For chemotherapy-naïve and previously
treated patients, the median survival from the start of HAI
therapy was 50.8 and 35months, respectively.
In our center we treated 36 patients with extensive
non-resectable CRLM (≥4 LM in 86%; bilobar LM in 91%)
using HAIC with oxaliplatin (100 mg/m2 in 2 hours) plus
intravenous 5-FU-leucovorin (LV: 400 mg/m2 in 2 hours;
FU: 400 mg/m2 bolus, then 2,400 mg/m2 in 46 hours), and
cetuximab (400mg/m2, then 250mg/m2/week, or 500mg/m2
every 2 weeks) as rst-line treatment.26 Overall response rate
was 90% (95% CI, 70–99) and disease control rate was 100%
(95% CI, 84–100). Forty-eight percent of patients were downstaged to R0 resection and/or radiofrequency ablation. Aer
a median follow-up of 11 months, median progression-free
survival was 20months (median overall survival, not reached;
12- and 18-month overall survival,100%).
HAIC has demonstrated promising results in the adjuvant
setting, where 44 of 98 patients were treated with postoperative oxaliplatin HAIC combined with systemic 5-FU and 54
(55%) aer curative resection of at least four CRLMs.27 e
median number of HAIC cycles administered per patient was
seven (range, 1–12). Twenty-nine patients (66%) had received
at least six cycles of HAIC with oxaliplatin, and 22 patients
(50%) had received the full planned treatment. For the remaining 22 patients (50%), HAIC chemotherapy had been discontinued because of toxicity (n=8), HAIC catheter dysfunction
(n=6), an early recurrence (n=6), and the patient’s refusal
(n = 2). While the two groups were similar in terms of age,
sex, and the stage of the primary, 3-year overall survival was
slightly higher in the HAIC group (75% vs. 62%, P = 0.17),
and 3-year disease-free survival was signicantly longer in the
HAIC group than in the IV group (33% vs. 5%, P<0.0001). In
the multivariate analysis, adjuvant HAIC and an R0 resection
margin status were the only independent predictive factors for
prolonged disease-free survival.
e benet aorded by HAIC in the adjuvant setting has
been conrmed in a prospective study of 287 patients with
liver metastases from colorectal cancer who were randomly
assigned to receive two cycles of HAIC plus four cycles of systemic chemotherapy or six cycles of systemic chemotherapy
alone aer curative resection of colorectal liver metastases.28
e HAIC and systemic chemotherapy regimens consisted of
a 2-hour infusion of oxaliplatin (85mg/m2) on day 1 and then
folinic acid, 200mg/m2, and 5-FU 2,400mg/m2 on days 2 and
3. e group receiving HAIC enjoyed signicant benets in
3-year disease-free survival (75.00% vs. 63.27%; P = 0.0035),
overall survival (84.29% vs. 65.31%; P = 0.0006) and liver
metastasis-free survival (80.00% vs. 69.39%; P=0.0451).
Improvement in HAIC has taken advantage of the technical breakthrough of percutaneous port-catheter implantation, to be proposed early in the disease and in borderline
surgical candidates, where a massive response is needed to
convert them to surgery. Today drugs injected in the hepatic
artery are the ones used IV while some compounds might be
more appropriate for HAIC, and development and research
are needed in this eld. Some preclinical studies have demonstrated benet of HAI injection of vascular endothelial
growth factor or endothelial growth factor inhibitors in a
rat model of CRLMs:when oxaliplatin alone was not capable of inhibiting tumor growth, HAIC with cetuximab or
bevacizumab signicantly reduced tumor tissue (P< 0.05).
Moreover, HAIC with cetuximab plus bevacizumab combined with oxaliplatin inhibited even more tumor growth.29
Such HAI-targeted therapy will probably soon be explored in
clinical studies.
Venous catheters andports
Externalized central venous catheters and totally implantable
central venous access port systems are widely used to improve
venous access reliability in patients receiving a prolonged
course of cytotoxic therapy, anti-infectious chemotherapy, or
long-term parenteral nutrition. Totally implantable venous
access port systems have several advantages over externalized
catheters, including reliable venous access, low incidence of
infection, absence of maintenance, and fewer restrictions on
activities, such as bathing and sports. Ports are usually inserted
by surgeons, anesthesiologists, or radiologists.
Description
ese devices consist of a port made of titanium or plastic with
a self-sealing septum, accessible by percutaneous needle puncture, and a radiopaque catheter usually made in a well-tolerated
long-term substance, silicone or polyurethane. Most ports are
288