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234
S. Kumar and G. N. Komalamma
artery on CT is 29mm and of the right interlobar artery is 17 mm [32]. The presentation of pulmonary artery aneu­rysms is often nonspecic, and many patients may not exhibit any symptoms. Some patients experience chest pain, short­ness of breath, hemoptysis, or superior vena cava (SVC) syn­drome [33].
Pulmonary artery aneurysms (PAA) can either be con­genital or acquired and are frequently diagnosed incidentally on imaging. However, in cases in which PAA is suspected, pulmonary angiography is considered the gold standard for diagnosis. This diagnostic method is effective in distinguish­ing PAA from other vascular abnormalities, such as pulmo­nary arteriovenous malformation (AVM). Other less invasive alternatives for diagnosis include CT, MRI, and echocar­diography. Among the complications of PAAs, dissection and rupture are the most severe and life-threatening.
Pulmonary artery pseudoaneurysms (PAPA) are nearly always acquired [34]. They are rare serious vascular abnor­malities that may represent a life-threatening condition, mainly due to Staphylococcus, Streptococcus, or Mycobacterium tuberculosis.
20.4.1 Endovascular Management
Embolization is the treatment of choice for peripheral aneu­rysms as the risk of sacricing adjacent normal lungs is min­imal, whereas, in central aneurysms, surgery is a better option (Fig. 20.7). Whenever possible, endovascular treat­ment is the primary approach, as it has the benet of reduced morbidity and mortality as compared to surgical treatment options. Endovascular therapy is best suited for saccular PAA or PAPA, both in the central and peripheral pulmonary
arteries [35]. Symptomatic and large true aneurysms and all pseudoaneurysms require treatment.
Coil embolization within the aneurysm itself offers the advantage of preserving the pulmonary arteries beyond the aneurysm, thus safeguarding the pulmonary function [36]. Stent-assisted coil embolization placing a bare-metal stent within the parent vessel to maintain its patency, followed by coil placement within the aneurysm [37]. N-butyl cyanoac­rylate (NBCA) glue has been reported to be used for the treatment of a bronchopulmonary shunt and PAPAs. NBCA is used with concomitant balloon occlusion of the pulmonary artery during injection to prevent distal embolization [38–41].
20.4.1.1 Technique
It is similar to the technique of embolization of PAVM. Access to the right common femoral vein is obtained and a 5 F angled pigtail catheter is advanced through the right atrium and ventricle into the main pul­monary trunk. Pulmonary manometry is performed to look for pulmonary hypertension. Subsequently, a 7 F long sheath is inserted into the central main pulmonary artery. Pulmonary angiography is then performed to visualize all pulmonary artery branches and perfusion in all lobes. Once the location of the aneurysm is ascertained, a selective catheter is employed to access the culprit pulmonary artery branch. Through gentle hand angiography, the aneurysm is visualized, and it is compared with the ndings in the CT scan. The catheter is then guided into the aneurysm, and coil embolization is performed. Subsequent angiography is checked to visualize any signicant residual lling within the aneurysm, and maintenance of perfusion in the peripheral branches.
20 Interventions ofthePulmonary Arteries
235
Fig. 20.7 Pulmonary artery aneurysm. (a) Chest X-ray showing ill-dened homogeneous radiopacity in the right lower zone; (b) selective DSA run of the right lower lobe segmental pulmonary artery showing saccular aneurysm; (c) glue embolization of the aneurysm sac; (d) post glue embolization runs showing complete thrombosis of the aneurysm sac
a b
c d

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doi.org/10.1016/j.rmcr.2015.08.003.

Hepatic Arterial Interventions

NavojitChatterjee andYashwantPatidar
21
Key Messages
1. Hepatic artery interventions are the standard of care for many hepatic pathologies.
2. Hepatic artery interventions are useful in vascular dis­ease as well as tumors of the liver.
3. Hepatocellular carcinoma (HCC) comprises the most common primary malignant tumor involving the liver.
4. Barcelona Clinic Liver Cancer (BCLC) system is the most widely used classication system for treatment planning and management of HCC.
5. Transarterial chemoembolization (TACE) involves selective injection of chemotherapeutic as well as embolic agents directly into the tumoral feeding artery, thus leading to tumor necrosis.
6. TACE is of two types: conventional TACE (cTACE) and drug-eluting bead TACE (DEB TACE).
7. Transarterial radioembolization (TARE) involves selec­tive injection of very small radioactive microspheres for treating the tumor cells.
8. Balloon occluded TACE (bTACE) is a newer technique and advancement of TACE.
9. Hepatic arterial interventions in post-transplant patients like hepatic artery thrombosis (HAT), hepatic artery ste­nosis (HAS), and hepatic artery pseudoaneurysm (HAP).
10. Hepatic parenchyma repopulation is a novel technique to increase hepatocellular regeneration.
liver parenchyma is from the portal vein (60–70%), the hepatic arterial branches are more expendable [1]. This, in addition to the fact that the majority of pathological entities of the liver receive their supply from the hepatic artery, makes hepatic artery interventions the standard of care for many hepatic pathologies.
Hepatic arterial interventions can be broadly classied into interventions for hepatic artery obstruction (stenosis/ thrombosis), interventions for abnormal hepatic artery dila­tation (aneurysm/pseudoaneurysm), interventions for abnor­mal hepatic artery communications (arterioportal stula, arteriovenous stula), interventions for benign and malig­nant liver lesions [hepatic arterial infusion chemotherapy (HAIC), transarterial embolization (TAE), transarterial che­moembolization (TACE), transarterial radioembolization (TARE)], interventions for the management of post­transplant arterial complications [hepatic artery thrombosis (HAT), hepatic artery stenosis (HAS), hepatic artery pseu­doaneurysm (HAP), hepatic artery rupture (HAR)], and novel interventions like liver parenchyma repopulation using hepatic stem/progenitor cells. The majority of our discussion will be focused on hepatic arterial interventions for HCC and non-HCC hepatic tumors.

21.2 Hepatic Arterial Anatomy

Proper knowledge of hepatic arterial anatomy is crucial prior

21.1 Introduction

Hepatic arterial interventions encompass a plethora of proce­dures that have been curated over the years to treat the major­ity of hepatocellular pathologies. The contrasting dual blood supply of the liver makes the liver parenchyma remarkably tolerant to ischemia. Since the predominant supply of normal
N. Chatterjee · Y. Patidar (*) Department of Interventional Radiology, Institute of Liver and Biliary Sciences, Delhi, India
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024 S. H. Chandrashekhara (ed.), Textbook of Interventional Radiology, https://doi.org/10.1007/978-981-97-9601-4_21
to performing hepatic arterial intervention, and a CT angiog­raphy is invariably used for procedure planning.
21.2.1 Normal Celiac Anatomy
The celiac artery most commonly gives its rst branch to the left gastric artery (LGA) and then bifurcates into a common hepatic artery (CHA) and a splenic artery (SpA). The CHA gives rise to the proper hepatic artery (PHA), gastroduodenal artery (GDA), and right gastric artery (RGA). The PHA gives
237
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N. Chatterjee and Y. Patidar
rise to the right (RHA) and left (LHA) hepatic artery branches, and the GDA gives rise to anterosuperior (ASPDA) and pos­terosuperior (PSPDA) pancreaticoduodenal arteries and the right gastroepiploic artery (RGEA). The SpA gives rise to the left gastroepiploic artery (LGEA), great pancreatic (GPA), and dorsal pancreatic (DPA) arteries and continues to supply
loop and then continues postero-lateral (horizontal) to give upper (segment VII) and lower (segment VI) branches. The LHA has a long horizontal segment that ends in an umbilical turn after which it continues anteriorly. At the umbilical point, it gives off the segment II branch while the anterior part gives off the segment III and segment IV branches.
the splenic parenchyma. Three major anastomoses involving the celiac trunk are seen along the lesser curvature of the stomach (RGA-LGA), greater curvature of the stomach
21.2.3 Variant Anatomies
(RGEA-LGEA), and head of the pancreas (SPDA—inferior pancreatic duodenal artery which is the rst branch of SMA).
Variant anatomies involving the celiac axis and hepatic arter­ies and their prevalence have been summarized in Table21.1.
21.2.2 Normal Hepatic Artery Anatomy
21.2.4 Extrahepatic Supply ofHCC
RHA gives rise to anterior and posterior sectoral branches. The anterior sectoral branch continues superiorly to the seg­ment VIII branch and gives small horizontal anterior segment V branches. The posterior sectoral branch forms a posterior
Table 21.1 Anatomical variations noted in the hepatic arterial supply
Celiac artery variants Hepatic artery variants Middle hepatic artery Extrahepatic supply HCC
Complete celiac trunk:
Normal anatomy (76%)
Incomplete celiac trunk:
One of the three branches does not originate from CA A) Gastrosplenic trunk: CHA does not originate from CA. B) Hepatosplenic trunk: LGA does not originate from CA. C) Hepatogastric trunk: SpA does not originate from CA. Absent celiac trunk: No common trunk. Each of the three vessels arises separately from the aorta or one branch arises from SMA
Complete celiacomesenteric trunk
CA+SMA have a common origin in the abdominal aorta (AA)
Incomplete celiacomesenteric trunk One branch of CA arises from AA with the rest arising as a common trunk with SMA A) Hepatosplenomesenteric trunk: Common trunk + LGA
origin from AA. B) Gastrosplenomesenteric trunk: Common trunk + CHA origin from AA.
Celiacomesenteric anastomosis: Persistent arc of
Buhler with direct anastomosis between CA and SMA
CA celiac artery, SMA superior mesenteric artery, LGA left gastric artery, AA abdominal aorta, CHA common hepatic artery, LHA left hepatic artery, RHA right hepatic artery, MHA middle hepatic artery, HCC hepatocellular carcinoma
Michel’s classication:
I—Normal anatomy (55%) II—Replaced LHA from LGA (10%) III—Replaced LHA from SMA (11%) IV—Replaced RHA+LHA (1%) V—Accessory LHA from LGA (8%) VI—Accessory RHA from SMA (7%) VII—Accessory RHA+LHA (1%) VIII—Replaced RHA/ LHA+ Accessory LHA/RHA (4%) IX—CHA from SMA (4.5%) X—CHA from LGA (0.5%)
Ghosh etal. I—MHA from RHA (anterior sectoral branch) with a normal branching pattern (37.6%) II—MHA from LHA (medial sectoral branch) with a normal branching pattern (33.3%) III—MHA from RHA (anterior sectoral branch) with accessory RHA (13.6%) IV—MHA from LHA (medial sectoral branch) with accessory LHA (11.2%) V—MHA from RHA (anterior sectoral branch) with accessory RHA and LHA (2.4%) VI—MHA from RHA (anterior sectoral branch) with CHA originating from SMA (1.2%)
HCC may sometimes derive vascular supply from nearby arter­ies that are not branches arising from the hepatic arterial trunk. Development of extrahepatic arterial supply to HCC occurs if
Right inferior phrenic artery (70–83%) Omental artery (13%) Left inferior phrenic artery (12%) Right internal mammary artery (8%) Left internal mammary artery (1%) Supra renal artery (9%) Right renal artery (4–12%) Intercostal artery (6–8%) Cystic artery (4%) Gastric artery (3–4%) Lumbar artery (2%) Superior mesenteric artery (0.7–1.5%)
21 Hepatic Arterial Interventions
239
the tumor is very large (>5cm) and is located in the bare area of the liver, if the tumor is exophytic, or if there is an extrahe­patic extension if there is a history of prior TACE or surgery. Identifying the extrahepatic arterial supply of HCC is impor­tant prior to a session of TACE/TARE because if not identied, a part of the HCC will remain untreated and will lead to a par­tial response. The various arteries implicated in extrahepatic arterial supply to HCC are summarized in Table21.1.
21.3 Hepatic Arterial Interventions forHepatocellular Carcinoma (HCC)
Hepatocellular carcinoma comprises the most common pri­mary malignant etiology involving the liver parenchyma [2]. Apart from the tumor characteristics, patient performance and liver function status play a crucial role in determining the treatment outcome in patients with HCC. Hence the Barcelona Clinic Liver Cancer (BCLC) system has been developed to customize therapeutic planning in HCC [3]. The new BCLC criteria with available treatment options are illustrated in Table21.2.
HCC receives almost the entirety of its blood supply from the hepatic arterial branches [4]. This fact can be utilized to selectively deliver chemotherapeutic/radioactive drugs to the tumor (with fewer systemic side effects). The culprit hepatic artery can also be selectively embolized to starve the tumor of its blood supply with minimal chances of liver infarction (due to patent perfusion by the portal vein). However, hepatic arterial interventions in HCC are not curative [5].
21.3.1 Transarterial Chemoembolization
(TACE)
TACE involves a selective injection of chemotherapeutic as well as embolic agents directly into the tumoral feeding artery. Selective injection permits the use of a lesser dose of the chemotherapeutic agent and hence fewer systemic side effects as compared to systemic chemotherapeutic drug injection. The process should be highly selective as an injec­tion into nontumoral hepatic artery branches may lead to arterial occlusion, hepatic ischemia, and biliary necrosis. (In contrast to the normal hepatic parenchyma which has a dual
Table 21.2 Simplied tabular depiction of Barcelona Clinic Liver Cancer (BCLC) 2022 [3]
BCLC stage Parameters Rx of choice Early (A)
Intermediate (B) Multinodular
Advanced (C) Portal invasion
TACE transarterial chemoembolization, TARE transarterial radioembolization
Single, or≤3 nodules each ≤3cm Preserved liver function, PS 0
Preserved liver function, PS 0
Extrahepatic spread Preserved liver function, PS 1–2
Therapeutic
1) Resection
2) Transplant
3) Ablation
1) Transplant—If ts the extended liver transplant criteria.
2) TAC E —Well-dened nodules with preserved portal ow.
3) Systemic chemotherapy—Diffuse extensive disease with bilobar involvement.
Systemic chemotherapy 1) TACE may be
Indication of arterial interventions TACE vs. TARE
Bridge to transplant if waiting period >6months
Downstaging to BCLC stage A (tumor shrinkage)
considered in patients with tumor thrombus in ipsilateral second- order or distal portal venous branches (VP1 and VP2—Liver cancer study group Japan).
No signicant data available for comparison
1) TACE is cheaper, and more available but requires multiple sitting.
2) TARE has a longer time to progress the tumor, decreased risks of complications, better tumor shrinkage, reduced hospital stay, and a similar overall survival rate as compared to TACE.
3) Due to less hepatotoxic effects and increased liver regeneration potential, TARE is better suited than TACE to treat large HCCs with less residual liver volume.
1) Tumor thrombus in rst-order portal vein branch, main portal trunk, and portal branches contralateral to the involved lobe (VP3 and VP4—Liver cancer study group Japan) is an absolute contraindication to TACE.
2) TARE is associated with minimal embolic effect and is preferred over TACE in patients with portal vein tumor thrombosis.
3) TARE has a better survival outcome as compared to sorafenib for patients with segmental portal venous tumor thrombosis (VP1/2).
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vascular supply, the hepatic artery is the sole vascular supply to the biliary system.) [6].
21.3.1.1 Indications: (See Table21.2)
1. Early disease (BCLC-A): In patients who are not candi- dates for surgical resection but are candidates for liver transplantation with lung transplant waitlist (> 6months) (bridge to transplant) [7]. Patients with early-stage HCC with poor clinical features make curative therapies not feasible (treatment stage migration strategy) [8].
2. Intermediate stage (BCLC-B): TACE is the treatment of choice for the down-staging of well-dened lesions with the preserved portal venous ow and feasible arterial access [9].
3. Advanced stage (BCLC-C): TACE causes embolization of the hepatic artery which leads to the development of signicant liver ischemia if there is concomitant portal venous tumor occlusion (PVTT). However, TACE can be done in HCC with segmental PVTT with collateral circu­lation development and preserved hepatic function (VP1 and VP2) [10].
21.3.1.2 Contraindications
1. Terminal stage HCC (BCLC-D): Performance status >2, end-stage liver function [3].
2. Advanced HCC (BCLC-C): Bilobar disease with tumoral involvement of >70% of normal liver parenchyma [3], extrahepatic extension [3], high-grade PVTT (Vp 3/4) [10].
21.3.1.3 Patient Selection
The STATE (selection for transarterial chemoembolization treatment) and the HAP (hepatoma arterial-embolization prognostic) scores are used for better patient selection prior to TACE [11] (Table21.4).
pumping actions) using a three-way stop cock so that emul­sion droplets attain a uniform small diameter and deposition in the tumor bed is homogeneous (Fig.21.1). Gelfoam slurry/ PVA particle (<300μ) is injected in the end to cause emboliza­tion at the capillary level within the tumor for longer retention of emulsion within the tumoral bed. It also causes hypoxia in the tumor cells which leads to the inactivation of P-glycoprotein pumps required for the expulsion of intracellular chemothera­peutic drugs (synergistic effect) [14]. Lipiodol deposited in normal liver parenchyma is metabolized by hepatocytes. However, cancer cells cannot metabolize lipiodol, and hence there is a long and sustained deposition of the emulsion within the tumor cells. Thus lipiodol helps in the selective delivery of the chemotherapeutic drug to the tumoral cells [15].
Drug-Eluting Bead TACE (DEB-TACE)
DEB is nega-
tively charged small (diameter <300μ) microspheres that can adsorb positively charged chemotherapeutic drugs (doxorubicin, irinotecan) on their surface by ion exchange principle [16]. They are not radio-opaque and have to be mixed with nonionic water-soluble iodinated contrast media (volumetric ratio of 1:3 for DEB:contrast). Being <300μ in diameter, they have deeper penetration and cause emboliza­tion at the capillary level with no spillage of the drug into the portal circulation (low systemic side effects). This also helps in a higher concentration of beads within the tumor. There is a slow and sustained release of chemotherapeutic agents within the tumor which complements the ischemic necrosis caused by embolization of the tumor vascular bed by the microspheres. However, the high embolism potential of microspheres may lead to a higher incidence of nontarget hepatic artery embolization, and ischemic necrosis of the liver and bile ducts (ischemic strictures, cholangiogram abscesses) [17]. The various agents used for DEB-TACE are summarized in Table21.3.
21.3.1.4 Patient Preparation
Systemic antiemetic and antibiotic prophylaxis are to be pro­vided prior to the procedure. Ceftriaxone (1g IV) is admin­istered 1hour prior to the start of the procedure. In cases with sphincter of Oddi incompetence (hepaticojejunostomy, trans-papillary biliary stent, sphincterotomy), oral moxiox­acin (400mg OD) is administered 3days prior to 17 days after the procedure [11]. TACE involves the placement of a 6F arterial sheath and hence has a low bleeding risk. In non­cirrhotics, a threshold INR of <2–3 and platelet count of >20×109/mm3 is advised [12].
21.3.1.5 Principle andProcedure
Conventional TACE (cTACE) Uses water in oil emulsion of chemotherapeutic drug-like epirubicin [water, 50–75mg] and lipiodol [oil, max dose—15–20ml] in a volumetric ratio of 1:1 (drug:lipiodol) [13]. Thorough mixing is done (at least 20
Balloon-Occluded TACE (bTACE) bTACE is a novel tech­nique that uses a microcatheter with an occlusion balloon on its tip for conventional (cTACE) drug delivery. After selec­tive cannulation of the feeding artery by the balloon micro­catheter, the balloon is inated prior to drug injection. Occlusion of the arterial lumen causes a reversal of ow in the arterial segment distal to the balloon. The reversal in hemodynamics prevents nontarget embolization of drugs into small hepatic arterial branches arising from the feeding artery distal to the site of balloon occlusion. Also, the bal­loon acts as a mechanical occlusion device preventing non­target embolization of drugs proximal to the site of occlusion. bTACE has shown promising results in preventing nontarget embolization into hepatic artery branches (both proximal and distal to the site of balloon occlusion), cholecystic artery (prevent post-TACE acute cholecystitis), and gastric arteries (prevent post-TACE acute gastroenteritis) [18].
21 Hepatic Arterial Interventions
241
Fig. 21.1 Drug preparation in conventional transarterial chemoembolization (cTACE). (a) Epirubicin (50mg in 10ml) (arrow) and lipoidol (block) are taken in 1:1 ratio (ideally 1:2 ratio) in two separate plastic syringes. (b) They are mixed thoroughly using a three way [water (drug-arrow) in oil (lipoidol— block arrow) emulsion]. (c) The nal mixture should be homogeneous and have a bright orange color. (d) Simple pictorial depiction of TACE procedure. It involves cannulating the celiac trunk using a suitable catheter (Cobra 2 or Simmons) followed by selective cannulation and drug delivery into the branch of hepatic artery supplying the tumor. The point of drug delivery should be distal enough to avoid nontarget drug delivery and proximal enough to deliver drug into all the hepatic artery branches supplying the tumor
a
b
c d
The Endpoint of TACE Slow injection of the drug is performed (<1ml/ min) to prevent the formation of lipi­odol cast in the artery. The endpoint of chemoemboliza­tion is defined as stasis of the contrast column for two to five heartbeats. A subjective angiographic chemoemboli­zation endpoint (SACE) has been described which sug­gests minimal residual tumoral flow or blush (sub stasis—grade 2/3) improves post- embolization survival compared to complete stasis with no residual flow/ tumoral blush (grade 4) [19].
21.3.1.6 Response Evaluation
Triple phase CECT/CEMRI is used for response evaluation after TACE at 1–3 months. Evaluation is done using the modied RECIST criteria. TACE is repeated if there is a partial response or treatable tumor progression. The Japanese Society of Hepatology advocates switching to sys­temic chemotherapy if there is an insufcient response or tumor progression after two sessions of TACE [20]. The patients must undergo triple-phase CECT/CEMRI every
3–6 months if there is a complete response after TACE (Figs.21.2 and 21.3).
21.3.1.7 TACE Failure
TACE failure or refractoriness was dened by the Japanese Society of Hepatology by the following criteria [20]:
A) Insufcient response: More than 50% viable tumor after
> two consecutive sessions of TACE.
B) Tumor progression after > two consecutive sessions of
TACE. C) Continuous elevation of tumor markers after TACE. D) Untreatable progression: New-onset vascular invasion,
extrahepatic spread, metastasis after TACE.
21.3.1.8 TACE Discontinuation
The ART (Assessment of Re-treatment of TACE) score [21] and the ABCR (α-fetoprotein, BCLC, Child-Pugh, and Response) score [22] are used in between sessions of TACE regarding discontinuation (Table21.4).
242
Table 21.3 Comparison between conventional TACE (cTACE) and drug-eluting beads (DEB) TACE
Conventional TACE DEB TACE
Agents A) Chemotherapeutic drug: Cisplatin, doxorubicin,
Tumor labeling in follow-up CECT
Drug release Fast, nonsustained Sustained, targeted release Tumor response – Similar efcacy to cTACE Time to progression – Similar to cTACE Overall survival – Similar to cTACE Preferred scenario 1) Superselective catheterization cannot be achieved
Side effect prole Post-embolization syndrome is seen more commonly
TACE transarterial chemoembolization
Mitomycin. B) Lipoidol: (1) selective delivery of the chemotherapeutic agent to the tumor. (2) tumor microcirculation embolization. (3) post-treatment drug deposition. C) Gelfoam: Temporary distal occlusion of the artery feeding the tumor.
I—Compact, homogenous lipiodol deposition in tumor and peritumoral area II—Homogenous lipiodol deposition in the tumor alone III—Weak heterogeneous lipiodol deposition with lling defects IV—Very weak/no lipiodol deposition
with multiple arterial branches arising distal to the site of drug delivery.
2) Multifocal disease.
3) TACE + ablation (uoroscopic localization).
as compared to DEB-TACE (a more systemic chemotherapeutic drug)
A) Drug-eluting microspheres:
DC beads (100–300μ): PVA hydrogel + sulfonate Lumi beads: Radiopaque DC beads Hephasphere (30–60μ): PVA co-sodium acrylate +
hydrogel. Expand 4 times after loading (become nonspherical) Tandem beads (100μ): Sodium polymethyl acrylate hydrogel. Tightly calibrated beads (<5% size change). Maximum suspension time Life pearl (30–60μ): PEG hydrogel. Expand 4 times after loading (spherical with tight size calibration), wider drug loading options, and longer suspension time B) Drug: Doxorubicin—75mg (37.5mg/ml beads), loading time—45minutes Irinotecan (DEBIRI)—100mg, loading time—120min C) Iodinated contrast media: Fluoroscopic visualization.
No
1) Large tumor (>5cm).
2) Multiple arterial supplies.
Has a higher risk of nontarget hepatic artery embolization— Biliary necrosis and cholangiogram abscess
N. Chatterjee and Y. Patidar
21.3.1.9 Complications
1. Systemic chemotherapeutic effect: Post- chemoembolization syndrome—pain is the most common feature. (cTACE > DEB-TACE)
2. Nontarget embolization of hepatic artery: (a) Liver isch- emia—abscess, liver failure, hepatic encephalopathy; (b) biliary injury—ischemic biliary stricture, cholangiogram abscess. (DEB-TACE > cTACE)
3. Extrahepatic nontarget embolization: Gastroenteritis, cholecystitis.
21.3.2 Transarterial Radioembolization (TARE)
It involves a selective injection of very small radioactive microspheres for treating the tumor cells. As the particles are extremely small, they reach the capillary level and do not have any signicant embolic effect. Due to this reason, hepatic ischemia, which is a relatively common complica­tion seen in TACE, is relatively uncommon with TARE.
21.3.2.1 Indications: (See Table21.2)
1. Early disease (BCLC-A): Indications in early HCC are similar to TACE.No studies are available comparing the efcacy of the two modalities in early HCC.
2. Intermediate stage (BCLC-B): TACE is the treatment of choice for tumor down-staging as it is cheaper and easily available. However, TARE has a longer time to progress the tumor, a better safety prole, a better tumor shrink­age rate, and similar overall survival. Due to its better safety prole, TARE is preferred over TACE for larger tumor burdens with less residual functional liver paren­chyma [23].
3. Advanced stage (BCLC-C): TACE causes embolization of the hepatic artery which leads to the development of signicant liver ischemia if there is concomitant portal venous tumor occlusion (PVTT). Hence, TACE is contra­indicated in VP3 and VP4 diseases. TARE has no embo­lism effect and hence is preferred over TACE in patients with HCC and PVTT.It can be used even in patients with VP3 and VP4 diseases and has better overall survival out-
bc
21 Hepatic Arterial Interventions
a
def
243
Fig. 21.2 Conventional transarterial chemoembolization (cTACE). (a–c) Pre-procedure triple phase CECT abdomen depicting an isodense lesion (a) showing non-rim enhancement in the arterial phase (b) and washout with a peripheral enhancing capsule in the portovenous phase (c)—suggestive of an LR-5 lesion (arrow). (d) Selective digital subtrac­tion angiography from posterior sectoral branch of the right hepatic
comes as compared to systemic sorafenib therapy in VP1 and VP2 diseases [23].
21.3.2.2 Contraindications [24]
1. Performance status >2
2. Tumor involving >70% of total liver volume
3. Bilobar multifocal disease with deranged liver function
4. Lung radiation dose of more than 30Gy per treatment, accumulated lung radiation dose of more than 50Gy
5. Lung shunt fraction of more than 20% (SIR sphere)
21.3.2.3 Agents Used
A beta-emitting radiolabeled (Yttrium-90, Iodine-131, Rhenium-188) microsphere is used for TARE. The micro­sphere is very small, has no macro embolic effect, and reaches the capillary level. It is made of glass (Therasphere) or resin (SIR sphere). A detailed comparison of Thermosphere and SIRsphere is made in Table21.5 [25].
21.3.2.4 First Visit (Planning)
1. Diagnostic angiography: Aortic, celiac, and SMA angio- gram is done to delineate abdominal vasculature and to
artery shows tumoral blush (curved arrow) with multiple intratumoral tortuous branches. (e and f) Post-procedure 1-month follow-up CECT triple phase abdomen shows a type 1 pattern of lipoidol deposition in the tumor in the noncontrast images (e). No enhancing areas are noted in the arterial phase images (f)—suggestive of LR TR—nonviable lesion (arrow)
rule out anatomic variants and extrahepatic supply to the tumor. Angiography from a hepatic artery is done to look for cholecystic and left gastric artery origin. Coil emboli­zation of these arteries may be prophylactically done if nontarget embolization in these branches is anticipated.
2. Technetium 99 m-macro aggregated albumin (Tc-MAA) SPECT CT: Tc-MAA (4–5mCi) is injected in the hepatic artery from where microsphere injection is anticipated. Tc-MAA scan is used to calculate lung shunt fraction, predict response, and radiation dose calculation.
3. Lung shunt fraction (LSF) calculation: Intratumoral arte- riovenous stulas are commonly associated with HCC and predispose to the shunting of hepatic arterial blood into pulmonary circulation. This may lead to the shunting of injected radioactive microsphere into the pulmonary circulation leading to radiation pneumonitis. A lung shunt fraction calculation is essential prior to microsphere injection. A lung radiation dose of more than 30Gy per treatment, and an accumulated lung radiation dose of more than 50Gy predispose to the development of radia­tion pneumonitis. For resin microspheres, a lung shunt fraction of 10–20% requires microsphere dose reduction,
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