21.3.2.5 Second Visit (Microsphere Injection)

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Fig. 21.3 Combined conventional transarterial chemoembolization (cTACE) and radio frequency ablation (RFA). (a and b) Pre-procedure triple phase CECT abdomen depicting a non-rim enhancing lesion (~4cm) in the arterial phase (a) showing washout with a peripheral enhancing capsule in the portovenous phase (b)—suggestive of an LR-5 lesion (arrow). The proximity of the lesion to right portal vein branch (block arrow) makes treatment using ablation alone very challenging (due to heat sink effect). (c) Selective digital subtraction angiography from posterior sectoral branch of the right hepatic artery shows

Table 21.4 Various pre- and post-TACE prognostication scores

STATE score HAP score ART score ABCR score

Use Patient selection for

Tumor load prior to treatment

AFP – >400ng/ml (1pt) – >200ng/ml: 1pt Albumin Baseline (g/dl) Bilirubin CRP – – – – BCLC – – – A: 0pt.

CTP – – Increase by 1: 1.5pt.

AST – – >25% increase: 4pt Radiological tumor

response Score Score>2.5s/o ineffective

TACE transarterial chemoembolization, STATE selection for transarterial chemoembolization treatment, HAP hepatoma arterial- embolization prognostic, ART assessment of retreatment of TACE, ABCR α-fetoprotein, BCLC Child-Pugh, and Response

TACE (baseline values) Beyond Ut7 criteria

(−12pt)

>1g/dl (−12pt)

– – No response: 1pt

Patient selection for TACE (baseline values)

Max diameter>7cm (1pt)

>37μmol/L (1pt) <36g/dl (1pt) – –

tumoral blush (curved arrow). (d) cTACE was done and homogeneous lipoidol deposition is seen in the entirety of the tumor (Type I) (arrow). Multitined RFA probe (block arrow) was placed in the lesion under USG and uoroscopy guidance. Lipoidol deposition makes probe placement easier and reduces the risk of post-RFA bleeding. (e and f) Post-procedure 1-month follow-up CECT triple phase abdomen shows a type 1 pattern of lipoidol deposition in the tumor with no enhancing areas in the arterial phase images (E)—suggestive of LR TR—nonviable lesion

Patient evaluation after TACE (post TACE values)

– –

Increase by ≥2: 3pt.

TAC E

Patient evaluation after TACE (post TACE values)

B: 2pt. C: 3pt

Increase by ≥2: 2pt

Response: −3pt

Score>4s/o ineffective TAC E

21 Hepatic Arterial Interventions

Table 21.5 Comparison between the two most common radio embolic agents used in TARE

Y90-Thermosphere Y90-SIR sphere Material Glass Resin Diameter (μ) Radiation dose /particle (Bq) 2500 50 Total number of particles used 1.2 million 40–80 million Total radiation dose 3GBq 3GBq Embolic effect Less More Microsphere dose D=A × 50 × (1-LSF) × (1-R)/m where

Advantages 1) Better suited for use in cases where a less embolic

Disadvantages Less effective in large lesions 1) Requires slow and controlled injection.

Y90 Yttrium cellular carcinoma

, TARE transarterial radioembolization, μ micrometers, Bq Becquerel, GBq GigaBecquerel, Gy Gray, m2 square meter, HCC hepato-

20–30 20–60

D(Gy)=Total dose administered, A(GBq)=activity

to be administered to target area, LSF=lung shunt

fraction, R=residual activity

effect is desired (e.g., HCC with deranged liver

parameters, HCC with portal vein tumor thrombosis).

2) Fewer chances of reux (less biliary/gastric

complications after the procedure).

A=BSA − 0.2+(% T/100) where A(GBq)=Total activity, BSA(m %T=percentage of liver involved by the tumor

Better suited for larger lesions

2) More chances of post-procedure liver failure and reux-related complications.

)=body surface area,

245

while a lung shunt fraction of more than 20% is a contraindication.

4. Radiation dose calculation: Formulae for glass and resin sphere dose calculation are shown in Table21.5.

21.3.2.5 Second Visit (Microsphere Injection)

The microsphere has to be injected within four weeks of the rst visit. It has a good safety prole and can be done as a daycare procedure. For patients with solitary lesions and normal liver function, lobar injection of the microsphere may be done. For solitary lesions with abnormal liver function, a segmental injection is done. For multiple lesions with preserved liver function, sequential lobar injection is done. TARE is contraindicated in patients with multiple liver lesions with deranged liver function.

21.3.2.6 Complications

1. Post-radioembolization syndrome: It is the most common complication (~30–50%). Fatigue is the most common presentation.

2. Radiation to normal liver parenchyma: Liver failure, radiation-induced liver disease (~5%).

3. Reux of microsphere: Biliary complications (~10%), gastric complications (~5%).

4. Lung shunting: Radiation-induced pneumonia (<1%).

21.3.4 Hepatic Artery Infusion Chemotherapy (HAIC)

HAIC involves the direct delivery of a chemotherapeutic agent to the liver with a catheter tip in the common hepatic artery. There is high rst-pass metabolism of the chemotherapeutic agent by the liver before it reaches the systemic circulation and hence has lesser systemic side effects as compared to systemic chemotherapy. A high concentration of chemotherapeutic drugs can be delivered to the HCC with no signicant increase in systemic toxicity. HAIC is indicated in advanced HCC (BCLC-C) where TACE and TARE are contraindicated and have shown a better overall survival rate as compared to systemic chemotherapy [27].

21.4 Hepatic Arterial Interventions inNonHCC Liver Tumors

Non-HCC liver tumors comprise a vast spectrum of tumors including benign tumors (like hemangioma, FNH, and adenoma), intrahepatic cholangiocarcinoma (IHCC), and liver metastasis from colorectal carcinoma (CRC), breast, melanoma and neuroendocrine tumors (NET).

21.3.3 Transarterial Bland Embolization (TAE)

Bland embolization is done using gel foam or PVA particles and acts by depriving the tumor of its arterial blood supply. It is a simple procedure and is indicated only in the setting of a ruptured nonresectable HCC in a hemodynamically unstable patient [26].

21.4.1 Neuroendocrine Liver Metastasis (NELM)

Neuroendocrine tumors very commonly metastasize to the liver (80%). The treatment modality for NELM is decided based on liver tumor load, pathological grade of the tumor (WHO Gd-I to Gd-III based on Ki67, mitotic count, and differentiation), and degree of endocrine activ-

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ity. Curative surgical resection is the treatment of choice for patients who are t for surgery with well-dened resectable liver metastasis (no lymph nodal, extrahepatic, or peritoneal metastasis). Liver transplant is not routinely done due to the high recurrence rate. Hepatic arterial interventions and percutaneous ablation are reserved for unresectable liver metastasis (30–50% liver invasion) with low pathological grade (WHO Gd-I and Gd-II) [28]. Hepatic arterial intervention in this setting is not curative and benets the patient only by controlling growth and endocrine symptoms. Bland embolization and conventional TACE are well tolerated by patients as compared to DEB-TACE and TARE (associated with increased incidence of acute carcinoid syndrome, complications, and death) [29]. Bland embolization has better outcomes in cases of liver metastasis from gastrointestinal NET while cTACE (Cisplatin + doxorubicin) has better outcomes in cases with liver metastasis from pancreatic NET [30]. Poor overall survivability is seen if the location of primary NET is unknown, higher pathological grade (WHO Gd-III), in male patients and in NELM of the caudate lobe [31]. Increased risk of acute carcinoid syndrome is seen after the episode of embolization if there is associated portal venous thrombosis and bile duct dilatation. In advanced unresectable diseases, hormonal (octreotide), conventional (Cisplatin), and targeted molecular (peptide receptor radionuclide therapy—PRRT) chemotherapy may be of value. Cytoreductive surgery is indicated if symptoms are not controlled using drug/hormonal therapy.

21.4.2 Other Liver Metastases

are inoperable at the time of presentation. IHCC is chemoresistant and causes satellite metastatic liver lesions making systemic chemotherapy and liver transplantation ineffective therapies. The majority of mortality in latestage IHCC is due to intrahepatic tumor burden (liver failure), and hence liver-directed therapies are the cornerstone of treatment for unresectable IHCC and increase overall survival even in patients with extrahepatic metastasis. The location and vascularity of the tumor dictate therapeutic planning. A hypovascular tumor is managed more efciently with percutaneous ablation or external beam radiotherapy (EBRT) while hypervascular lesions are better managed using hepatic arterial interventions. Patients undergoing TARE have a better response (mRECIST) as compared to TACE (conventional/DEB) and TAE [33].

21.4.4 Benign Liver Tumors

Various benign pathologies like hemangioma, adenoma, focal nodular hyperplasia (FNH), and benign hepatic cysts (ADPKD) may involve the liver parenchyma. Most of these lesions are asymptomatic and may be managed conservatively. Treatment is warranted if the lesions become symptomatic, start enlarging in size, cause hemorrhage, hepatic insufciency, or show a malignant transformation [34]. Surgical resection is the mainstay of therapy. Interventional radiological treatment can be used in cases where surgery is not feasible or as a presurgical treatment (reduction in size or vascularity). Intervention radiological strategies may include percutaneous ablation or hepatic arterial embolization (bland embolization or conventional chemoembolization).

Most commonly originate from colorectal carcinoma (CRC), breast, and melanoma. The oligometastatic disease has been successfully treated using percutaneous ablative therapies as well as hepatic arterial interventions. DEBIRI TACE has shown much promise in the treatment of CRC liver metastasis [32]. Patients with oligometastatic breast cancer disease (few metastases conned to the liver) have shown more survival after DEB-TACE as compared to conventional TACE.

21.4.3 Intrahepatic Cholangiocarcinoma (IHCC)

IHCC is the second most common primary liver malignancy. Ten percent of cholangiocarcinoma is intrahepatic, and the majority of IHCC presents as mass-forming lesions. The tumor is inltrative in nature and presents at a more advanced stage, hence the majority of the lesions

21.4.4.1 Hemangiomas

They are the most common benign tumor involving the liver parenchyma. They are mostly managed conservatively (steroids, beta-blockers). Nonconservative management is warranted when the lesions are symptomatic, large in size (giant hemangiomas >10cm), and present with Kasabach Merritt syndrome, rupture, and hemorrhage. Surgical resection is the rst treatment modality. Transarterial bland embolization (TAE) may be done prior to surgery (to reduce size and vascularity) or in cases of tumor rupture. cTACE using bleomycin and lipiodol mixture may also be done [35]. (Fig.21.4) Percutaneous RFA is also a treatment option.

21.4.4.2 Focal Nodular Hyperplasia

This is the second most common benign liver lesion and is characterized by a central stellate scar with an artery traversing through the scar. Treatment is indicated in growing lesions and large (>4cm) lesions with a suspected increased

21 Hepatic Arterial Interventions

abc

de f

247

Fig. 21.4 Transarterial chemoembolization (cTACE) using bleomycin and lipoidol mixture for giant hemangiomas. (a and b) Pre-procedure triple phase CEMRI abdomen: T2 weighted image (a) depicting two large T2 hyperintense lesions with areas of very bright T2 signal areas within. Arterial phase post-contrast T1 weighted fat saturation image (b) showing globular discontinuous peripheral puddles of enhancement (arrows) in both the lesions—ndings suggestive of giant hemangiomas. (c) Selective digital subtraction angiography from posterior sectoral branch of the right hepatic artery (block arrow) shows this artery

risk of traumatic hemorrhage [36]. TAE may be done prior to surgery or as an alternative to surgery.

21.4.4.3 Hepatocellular Adenoma

It is the third most common benign liver tumor and has a high propensity to hemorrhage. Tumor growth is associated with oral contraceptive pill use and pregnancy (estrogen- dependent). For symptomatic patients with tumor rupture, surgical resection is the treatment of choice for stable patients while TAE is the treatment of choice for unstable patients with hemoperitoneum. The rst line of treatment in asymptomatic patients is the removal of the offending agent (OCP) and reimaging after 3–6months. The lesion may be managed conservatively if it reduces or stays stable in size in the follow- up scan. Surgical resection is indicated after the follow- up scan if the lesion grows in size or if there is an increased risk of hemorrhage (>5cm) and malignant transformation (males, glycogen storage disorder) [37].

21.4.4.4 Polycystic Liver Disease

Hepatic cysts in ADPKD derive their blood supply from the hepatic artery. Shrinkage of cysts may occur after TAE.

is supplying the tumor with multiple areas of tumoral blush (arrow). (d) Post-TACE selective angiography from posterior sectoral branch of right hepatic artery shows lipoidol cast in the feeding artery with no tumoral blush. (e and f) Abdominal radiograph (e) and coronal reformat of arterial phase CECT abdomen (f) after multiple sessions of TACE (bleomycin + lipoidol) shows patchy peripheral deposition of lipoidol (arrows). There is no residual arterial phase enhancement in the right lobe lesion. However, few areas of residual arterial phase enhancement are seen in the left lobe lesion

21.5 Hepatic Arterial Interventions inPostTransplant Patients

Hepatic arterial complications comprise the most common vascular complications in a post-liver transplant patient. The hepatic artery provides the major blood supply to the hepatic parenchyma and bile ducts in a post-transplant liver, and hence hepatic arterial complications pose a serious threat to graft function and recipient survivability. Cholangiolar abscesses and nonanastomotic biliary strictures are more commonly seen in recipients with hepatic artery complications. Arterial complications are more commonly seen in adult patients and occur equally in live donor liver transplants (LDLT) and dead donor liver transplants (DDLT) (unlike venous complications which are more common in the pediatric population and LDLT). Diagnosis is made using a Doppler study. Various hepatic arterial complications are tabulated in Table21.6.

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Table 21.6 Common hepatic arterial complications associated with liver transplantation and their management

Trivia Clinical feature Risk factors Treatment

Hepatic artery thrombosis (HAT)

Hepatic artery stenosis (HAS)

Hepatic artery pseudoaneurysm (HAP)

Hepatic artery rupture (HAR)

LDLT live donor liver transplantation, DDLT dead donor liver transplantation, LFT liver function tests, TACE transarterial chemoembolization, RxOC treatment of choice

Most common arterial complication, most severe complication, a most common cause of death and graft loss

HAP progresses to HAR Early>Late

Early>Late

Adult > child LDLT >DDLT Early—Graft dysfunction Late—Ischemic cholangiopathy

Late>Early

Asymptomatic with raised LFT

Early>Late

High mortality

MC- surgery- related Nonsurgical factors: Old age, prior TACE, hypercoagulable state, ABO incompatibility

Surgery related Excessive length of donor artery, donor–recipient vessel caliber discrepancy

Peritoneal infections (fungal)

Fungal infection RxOC—

N. Chatterjee and Y. Patidar

RxOC—Retransplant

Intra-arterial thrombolysis is done when retransplant is not feasible

RxOC— Angioplasty±stenting

Surgical revision was done if the arterial intervention fails

RxOC—Covered stent placement

Urgent hepatic artery ligation was done if the arterial intervention fails

Embolization±Covered stent

Urgent hepatic artery ligation was done if the arterial intervention fails

21.6 Interventions inHepatic Artery Aneurysms andPseudoaneurysms

True aneurysms of the hepatic artery are less commonly seen compared to pseudoaneurysms. They are ow-related and more commonly seen involving major arterial trunks like common and proper hepatic arteries. They form due to a deciency in arterial wall strength and are more commonly seen in older patients (associated with atherosclerosis). If seen in younger patients, they may be associated with connective tissue disorders. Since true aneurysms are located in larger, nontortuous arteries (feasible for larger device placement) which are nonexpendable, placement of

a covered stent to cut off the aneurysm from the main circulation is the treatment of choice. If covered stent placement is not feasible, coil packing of the aneurysmal sac using detachable coils or balloon-occluded coil packing may be done [38].

Pseudoaneurysms of the hepatic artery are more common and are iatrogenic or infective in origin (MC—postintervention). They arise from segmental hepatic artery branches, lack all three wall layers, and require emergency intervention. Since they are located distally in expendable arteries with collateral circulation, the sandwich technique of coiling (closing both the backdoor and front door) is the treatment of choice (Fig.21.5).

21 Hepatic Arterial Interventions

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def

Fig. 21.5 Coil packing of hepatic artery pseudoaneurysm. (a) Coronal MIP reformat of CT angiography of the abdomen depicts a wide neck pseudoaneurysm arising eccentrically from the segment VIII branch of the right hepatic artery. (b) Selective right hepatic artery DSA images show the wide neck aneurysm arising from the proximal segment VIII branch. (c) The neck of the pseudoaneurysm was cannulated using a microcatheter and packing of the aneurysm sac was done using microcoils (block arrow). (d) Post-aneurysmal sac coil packing selective right hepatic artery DSA images show no contrast opacication of the pseudoaneurysm with patent distal ow in the segment VIII hepatic

21.7 Interventions inArterioportal Fistulas

Arterioportal stulas (APF) are more commonly acquired vascular malformations with direct communication between the hepatic artery and portal vein. An acquired arterioportal stula develops due to trauma, post-hepatic interventions, post-surgery, and spontaneously (e.g., in HCC). Arterioportal stulas are classied according to location and hemodynamics [39]. Type 1 arterioportal stulas are small peripherally located asymptomatic stulas. They develop mostly after hepatic interventions. They thrombose spontaneously and are managed conservatively. Persistence of ow after one month or development of symptoms warrants embolization. Type 2 arterioportal stulas are acquired large centrally located stulas which develop after penetrating liver lacerations. They present with features of portal hypertension and may lead to portal brosis if left untreated. Coil embolization is the rst line of

artery branch (arrow). Note the microcoils in the aneurysm sac (block arrow). (e) Post-procedure celiac angiogram shows no opacication of the pseudoaneurysm (coil packed—block arrow) with distal ow present in the segment VIII branch of the right hepatic artery (arrow). No other branches of celiac artery supply the pseudoaneurysm. No other pseudoaneurysms are seen. (f) Post-procedure coronal MIP reformat of CT angiography of the abdomen depicts metal artifacts in the pseudoaneurysm sac (block white arrow) due to microcoils. No contrast opacication of the pseudoaneurysm sac is seen with normal contrast opacication of the distal segment VIII hepatic arterial branch (white arrow)

treatment. PVA/glue embolization may be required if multiple feeders are present. Surgery is done if there is the persistence of ow after embolization. Type 3 arterioportal stula is congenital diffuse intrahepatic arterioportal communication. The baby presents with failure to thrive, severe portal hypertension, and cirrhosis. A liver transplant is the treatment of choice.

21.8 Hepatic Parenchyma Repopulation

Hepatic arterial infusion of bone marrow stem cells has been used as a novel technique to increase hepatocellular regeneration. This novel modality has been used for increasing liver regeneration in patients with cirrhosis [40]. This may also be used to increase liver regeneration in patients who fail to reach desired standardized future liver remnant (sFLR) after portal vein embolization.

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Interventions oftheHepatic Veins, Inferior Vena Cava, andPortal Vein

RanjanKumarPatel andAmarMukund

Key Messages

1. TJLB is a low bleeding-risk procedure, and the two most common indications for TJLB are coagulopathy and signicant ascites.

2. The two most common indications of TIPS in clinical practice are refractory ascites and secondary prophylaxis of variceal bleeding. Hepatic encephalopathy (HE) is the most common post-TIPS complication, seen in 25–45% of cases. Careful patient selection is crucial to prevent this complication.

3. TIPS vs. BRTO should be individualized depending on the vascular anatomy, associated co-morbidities, availability, and local expertise. TIPS may be a better option in patients with associated ascites and/or portal vein thrombosis without any other contraindications. In contrast, BRTO may be a good option for patients having a high risk of post-TIPS hepatic encephalopathy or heart failure.

4. PVR-TIPS may need procedure modications, such as transhepatic or transsplenic balloon or snare-assisted techniques.

5. A stepwise approach is followed in managing BCS, starting from anticoagulation, angioplasty ± stenting, creation of portosystemic shunt, and nally, liver transplantation.

6. Primary stenting in BCS is preferred for long-segment HV or IVC stenosis or occlusion, while only angioplasty sufces for short-segment stricture.

7. The indications of TIPS/DIPS in BCS include an absence of any recanalizable hepatic veins, failure to respond to angioplasty and anticoagulation, and progressive disease despite successful angioplasty and/or stenting.

R. K. Patel Department of Radiodiagnosis, All India Institute of Medical Sciences, Bhubaneswar, India

A. Mukund ( Department of Interventional Radiology, Institute of Liver and Biliary Sciences, Delhi, India

8. PVE is a safe and well-tolerated procedure without any change or a slight transient uctuation in liver function following the procedure. Unlike trans-arterial embolization, patients experience either no or minimal postembolization syndrome because PVE induces apoptosis rather than ischemic necrosis.

9. PVE with glue induces superior FLR hypertrophy than other embolic agents; however, glue embolization requires technical expertise to avoid non-target embolization.

10. The most common indications for IVC lter placement in patients with VTE are contraindication to anticoagulants, failure to anticoagulants, and stoppage of anticoagulants due to complications.

22.1 Introduction

Interventional procedures of hepatic veins, inferior vena cava (IVC), and portal veins are mostly related to liver cirrhosis and portal hypertension. The different interventional procedures include basic procedures like transjugular liver biopsy and hepatic venous pressure gradient measurement to technically challenging procedures such as transjugular intrahepatic portosystemic shunt (TIPS) or direct IVC to portal vein shunt (DIPS). Patients with Budd–Chiari syndrome require hepatic vein or IVC angioplasty with/without stenting. Moreover, patients with dominant spontaneous portosystemic shunt-related symptoms (bleeding and hepatic encephalopathy) demand shunt occlusion, usually achieved through retrograde venous route, i.e., balloon or vascular plug-assisted retrograde transvenous obliteration (BRTO/ PARTO). As an alternative to portal vein ligation (PVL), portal vein embolization (PVE) can be performed in a minimally invasive way to achieve adequate future liver remnant hypertrophy, thereby avoiding liver failure following hepatectomy. This chapter describes each of the mentioned procedures in detail.

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R. K. Patel and A. Mukund

22.2 Transjugular Liver Biopsy (TJLB)

Transjugular liver biopsy (TJLB) is considered in patients with a diffuse liver disease where percutaneous liver biopsy is contraindicated or in conjunction with other procedures requiring transjugular access, such as hemodynamic monitoring and HVPG measurement, TIPS, or HV angioplasty. The two most common indications are coagulopathy and signicant ascites. Other indications include increased bleeding risk conditions, such as hereditary hemorrhagic telangiectasis, peliosis hepatis, suspected hepatic amyloidosis, or morbid obesity. Although not usually indicated, in some circumstances, TJLB may be considered for biopsy of the focal lesion in the vicinity of one of the hepatic veins [1, 2]. The diagnostic yield of TJLB ranges from 85 to 100% [3, 4].

The contraindications to TJLB are uncorrectable severe

coagulopathy and thrombosis of bilateral jugular veins.

22.2.1 Patient Preparation

A preliminary USG is done to conrm the patency of IJV, the diffuse nature of the liver disease, the amount of ascites, and most importantly, the patency of hepatic veins. It is advisable to drain moderate to gross ascites before the procedure. Although a low bleeding risk procedure, INR should be corrected to 2–3, and platelets should be transfused if <20,000/ mm3 [5].

22.2.2 Procedure

TJLB is performed in a uoroscopic suite under local anesthesia with or without conscious sedation. Intraprocedural vitals, oxygen saturation, and cardiac rhythm are monitored to detect tabletop complications.

Steps

• After USG-guided IJV access, the hepatic vein (HV) is

catheterized using a combination of a 5F multipurpose (MPA) catheter and a 0.035″ hydrophilic guidewire. Right HV is preferred as it has a relatively straighter course and the least acute angulation. Different-shaped catheters, such as C2 or reverse curve catheters, may be attempted in case of an acute angle of entry into HV.

• A hepatic venogram is taken after HV cannulation to deter-

mine its patency. Over the guidewire, an occlusion balloon catheter (Swan-Ganz catheter) is placed in the HV (within 1–3cm of IVC). Free HV and balloon- occluded HV pressure (~wedge HV pressure) are measured to calculate HVPG (hepatic venous pressure gradient) (Fig.22.1a). The difference between FHVP and IVC pressure at the level of HV conuence should be <2mm Hg.

• The hydrophilic guidewire is exchanged with a stiff

guidewire, and a 9F vascular sheath is advanced into the HV. The TJLB stiff cannula (LABS-100; Cook Inc., Bloomington, IN) is advanced within the sheath, and its tip is positioned 2–3 cm into the liver from the hepatic vein ostium. Breath-hold at deep inspiration may facilitate the negotiation of the stiff cannula into the HV.

• With the patient holding his breath, the stiff cannula is

turned (anteriorly if in the right hepatic vein and to the right if in the middle hepatic vein) to wedge against the liver parenchyma. The Tru-Cut biopsy needle (18/19G-60cm quick core biopsy needle) is advanced ahead of the stiffening cannula, and a biopsy is taken (Fig.22.1b).

• Usually, 3–4 passes are made for adequate samples [6]. A

specimen of either 15mm in length or containing at least six complete portal tracts is considered adequate [1–4].

• After the biopsy, a check hepatic venogram is done through

the sheath to exclude contrast extravasation, if any.

• Finally, the sheath is removed, and the IJV access site is

secured with compression.

Fig. 22.1 Transjugular liver biopsy (TJLB). (a) Balloonoccluded hepatic venogram (black arrow A) for WHVP measurement after RHV catheterization through the right jugular approach before measuring; (b) Transjugular liver biopsy under combined USG (open white arrow B) and uoroscopic guidance using LABS-100 set. IVC Inferior vena cava, RHV Right hepatic vein, WHVP Wedge hepatic venous pressure

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