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412
Fig. 37.3 A 16-year-old male
with a tibial osteoid osteoma
and severe pain relieved by
nonsteroidal antiinammatories. (a) Axial CT
images demonstrates a
cortical-based lucent lesion in
the medial tibial diaphysis
with surrounding sclerosis.
(b) Intra-procedural image
demonstrating a
radiofrequency probe placed
into the lesion
D. M. Mauro
between ablation modality, 4.5% for cryoablation and 4.3%
for radiofrequency ablation. In a 2014 study by Georgiades
etal., 134 patients underwent cryoablation for biopsy-proven
renal cell carcinoma with a median tumor size of 2.8 cm
[39]. They reported a 5-year cancer-specic survival of
100% and 5-year recurrence-free survival of 97%, results
that approach that of surgical therapy.
Bone Lesions
Percutaneous ablation has become the primary treatment
option for patients with osteoid osteoma given the high rate
of technical success and improved morbidity and complication prole compared to surgical curettage (Fig.37.3) [6].
The role of ablation in osseous metastatic disease is not
clearly dened but is frequently used as an adjunct for pain
palliation in patients who have failed conventional therapy,
in patients with oligometastatic disease who are poor candidates for conventional therapy, or for targeted lesions that
place the patient at high risk of future morbidity with tumoral
progression.
In a large meta-analysis involving 20 studies and 1356
patients, percutaneous radiofrequency ablation demonstrated
a 92% primary success rate in treating osteoid osteoma [40].
Secondary success rate has been reported to approach 100%
(99.6%) [41]. A literature review of 27 studies including
1772 patients concluded the average recurrence rate to be
4.9% [21]. Average complication rate across 13 studies was
shown to be 2.9% [40]. Both radiofrequency ablation and
cryoablation have been shown to have signicant pain reduction and decreased analgesic use [42–44].
After percutaneous ablation is chosen as the treatment
plan, typically via a multidisciplinary tumor board, the
patient should be seen in an outpatient interventional radiology clinic. A full medical history is taken and physical
exam is performed. The patient’s comorbidities, functional
status, and current medications should be reviewed to aid
in the discussion of procedural risk, patient expectations,
and sedation options. Pre-procedural imaging, most commonly CT or MRI, is reviewed to plan patient positioning
and access route. Recent laboratory tests are reviewed, or
new labs ordered, with special attention paid to renal function (for possible contrast administration and renal functional reserve) and coagulation. Institutional standards
should be followed in regard to laboratory value cutoffs.
According to SIR consensus guidelines, INR should be
less than 1.5 and platelet count >50,000 with radiofrequency ablation classied as category 2 (moderate risk of
bleeding) for straightforward procedures and category 3
(signicant risk for bleeding) for complex interventions
[45]. Patients are usually informed to be nil per os (NPO)
starting at midnight the day prior to the procedure for
sedation. Anticoagulants and antiplatelet medications
should be held in adherence to department or Society of
Interventional Radiology guidelines [45].
Ablation may be performed under moderate sedation or
with general anesthesia. Comorbidities, patient cooperation,
and radiologist preference drive this decision. Consideration
should be made for lesion location, ablation technology, and
expected procedure duration. Within the lung, treatment of
pleural-based lesions is more painful than parenchymal
lesions. Similarly, peripheral renal lesions tend to be more
painful than central lesions, likely due to capsular innervation. Overall, heat-based ablations tend to be more painful
than cryoablation. Additionally, there is a risk of nerve stimulation during radiofrequency ablation.
Ablation technology is chosen based on operator preference, availability, as well as lesion location and size.
The number of probes and ideal positioning will be determined by technology selection and vendor-specic ablation
parameters.
37 Lung, Kidney, andBone Ablation
The How To
1. Patient positioning is selected after reviewing pre-
the lesion(s) given the chosen imaging modality(s).
A route is chosen to avoid intervening structures.
Within the lung, a route is chosen to avoid ribs,
sels, and bronchi. For renal and hepatic ablation,
special attention is paid to the hilar vessels and urinary or biliary collecting system, respectively.
2. The ablation probe is advanced under real-time
ultrasound imaging and/or intermittent CT imaging
until the lesion is speared or bracketed. Some operators prefer to obtain a biopsy prior to ablation, in
which case a trocar needle is used with coaxial
placement of a biopsy device and subsequently the
ablation probe (refer to Chap. 41 for more informa-
tion on biopsies).
3. Ablation progress can be monitored with intermittent imaging with attention to development of intraprocedural complications such as pneumothorax or
hemorrhage.
4.
acquired to evaluate for immediate complications.
If a pneumothorax is present, aspiration or chest
tube placement should be considered based on size,
expansion rate, and patient exam. If hemorrhage is
present, the operator may choose to reimage after a
short interval to assess the bleeding rate and need
for further intervention.
5. For lung ablation, at least one post-procedural chest
Operators may choose to discharge the patient after
a few hours or observe the patient overnight.
Some lesions are not safe to ablate due to adjacent vital
structures. In these cases, air or liquid can be infused to displace the adjacent tissue and create a safe ablation zone. For
example, if a renal lesion is adjacent to the colon, a separate
needle can be placed adjacent to the lesion with inltration
of saline (hydrodissection) or air (pneumodissection) to displace the colon. Similarly, for pleural-based lesions, a pneumothorax can be intentionally created to displace the lesion
away from the mediastinum or parietal pleura. For central
renal lesions where there is concern for thermal damage to
the collecting system, a ureteral stent can be placed with
infusion of uid into the renal pelvis as a coolant to prevent
urothelial damage.
Patients are often proscribed anti-inammatory medication (i.e., ibuprofen) following the procedure for pain control
and to reduce incidence or severity of a systemic inammatory response. Oral opiate medications are often necessary
413
Table 37.4 Summary of complication rates for lung, kidney, and bone
ablation
Major complications (percentage)
Lung ablation (9.8) [46,
47]
Pneumothorax (46–52)
Requiring chest tube (21)
Pleural effusion (19) Hemorrhage (1.2–4.8) Pain
Hemoptysis (6) Nerve injury (1–6) Neuritis
Pleuritis (2.3) Pneumothorax (0–2) Adjacent
Pneumonia (1.8) Infection (<1) Abscess
Abscess (1.6) Tumor seeding (<<1) Seroma
Signicant bleeding (1.6) Urethral injury (leak,
Death (0.4) Colonic perforation
Bronchopleural stula
(0.4)
Brachial nerve injury (0.3) Decreased renal
Tumor seeding (0.1)
Diaphragmatic injury (0.1)
Renal ablation (4–6)
[48, 49]
Hematuria (10–20) Bleeding
stricture)
Adrenal crisis
function
Bone ablation
(3.3) [7]
structure
injury
Skin burn
for additional pain control. Pain, controlled by oral pain
medication, and 2–3 days of a low-grade fever are common
following ablation. Strenuous activity should be avoided for
2–3 days, at which point patients may return to normal activity. Some patients will develop post-ablation syndrome, a
transient, self-limited constellation of symptoms including
low-grade fever, malaise, body ache, and nausea. Symptom
duration varies based on the volume of tumor ablated, and
patients should be treated with nonsteroidal anti-inammatories and uids with symptoms generally lasting a week.
Patients should avoid air travel or scuba diving for at least
3weeks following lung ablation to avoid a delayed pneumothorax from changes in atmospheric pressure.
Major complication rates are relatively low for percutaneous ablation. Table 37.4 summarizes complication rates for
lung, kidney, and bone ablation with organ type and lesion
location playing a crucial role. Cryoablation and radiofrequency ablation have been shown to have similar complication rates for small renal mass ablation [38].
Follow-up imaging can be performed with either MRI,
CT, or positron emission tomography/computed tomography
(PET-CT) within 1–2 months after the procedure to establish
a post-procedure baseline and then at 3-month intervals for 1
year. After 1 year, annual surveillance is typically performed.
For lung ablation, there is a surrounding ground-glass halo
around the ablation site on post-procedure and early followup imaging [50]. A margin of at least 5 mm has demonstrated
improved outcomes. The ablation bed evolves over time;
small lucencies can develop and progress into cavitation.
The ablation zone will decrease in size with scarring. For
renal ablation, on 1–2-month follow-up imaging, the abla-
414
D. M. Mauro
tion zone should overlap the tumor location with an ablative
margin of 5–10 mm [51]. There is frequently benign periablation enhancement surrounding the ablation zone that
should be regular and symmetric and can persist up to 6
months. Irregular or nodular peripheral enhancement signies residual tumor or local tumor progression. Local tumor
progression can be visualized at any time point during postprocedure surveillance imaging. The ablation zone can have
central cavitation and will decrease in size and scar over
time. The ablation zone should never increase in size beyond
3 months following the procedure. Delayed increase in size
of the ablation zone indicates recurrence.
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Part X
Hepatobiliary Disease
Transjugular Intrahepatic Portosystemic
Shunt (TIPS) andPortal Hypertension
RohitKoppula andZivJHaskal
Pathophysiology
Chronic liver disease results in approximately 38,000
deaths a year, making it the 12th leading cause of mortality
in the United States [1]. Progressive liver disease results in
portal hypertension, the common endpoint of several pathologic processes which increase resistance to portal blood
ow. Portal hypertension can be classied as prehepatic,
intrahepatic, and post-hepatic (Fig.38.1) according to the
site of increased resistance. Cirrhosis is the most common
cause, accounting for 90% of cases. Additional etiologies
include bland or malignant portal vein thrombosis, hepatic
vein outow block, and inltrative or inammatory liver
diseases [2].
Worsening portal hypertension leads to refractory ascites,
hepatic encephalopathy, hepatic hydrothorax, hepatorenal
syndrome, and variceal hemorrhage. In combination with
endoscopic and pharmacologic treatments, the transjugular
intrahepatic portosystemic shunt (TIPS) is effective in treating
a variety of manifestations of portal hypertension.
It is important to quantify portal hypertension given its
prognostic implications for the development of ascites and
variceal bleeding. Classically, the portosystemic gradient
(PSG) is calculated as the difference between free hepatic
vein pressure (HVP) and wedged HVP. These values are
measured with a balloon-tipped catheter advanced into a
hepatic vein from a jugular or femoral access. The balloon
is used to occlude the hepatic vein, i.e., “wedging of the
R. Koppula
University of Virginia, Department of Radiology and Medical
Imaging, Charlottesville, VA, USA
e-mail: rk7ta@virginia.edu
Z. J Haskal (
University of Virginia School of Medicine, Department of
Radiology and Medical Imaging, Interventional Radiology
Division, Charlottesville, VA, USA
e-mail: ziv2@mac.com
*)
38
catheter” to block antegrade ow through the hepatic vein.
Wedged HVP is then measured at the catheter tip, which
reects the transmitted hepatic sinusoidal pressures and,
therefore, sinusoidal compliance [3]. This is analogous to
using a wedged pulmonary artery catheter to estimate left
atrial pressures. Free HVP pressure is obtained within the
hepatic vein with the balloon deated, approximately
2–4cm from the IVC-hepatic vein conuence. An elevated
free HVP can help identify post-hepatic causes of portal
hypertension, such as Budd-Chiari syndrome and tricuspid
regurgitation. The portosystemic gradient can provide an
accurate estimate of the actual or directly measured portal
pressure. Multiple studies have validated the portosystemic
gradient as a predictor of complications of portal hypertension in cirrhosis, and as an independent predictor of mortality (Table38.1) [4–8].
Key Point
Portosystemic gradient = wedged hepatic vein pressure – free hepatic vein pressure. A normal portosystemic gradient is 0–5 mmHg. An elevated gradient is
associated with complications of portal hypertension
and is an independent predictor of mortality.
Development of interstitial brosis and the formation of
regenerative nodules are important microscopic changes
which lead to cirrhosis. These changes disrupt normal
hepatic microarchitecture and result in narrowing of the
hepatic sinusoidal space, thereby increasing portal venous
pressures [9, 10]. Local production of vasoconstrictors in the
intrahepatic portal circulation is increased, as is arterial inow
to the splanchnic bed [11, 12]. Concurrently, there is dysregulation of sodium homeostasis leading to increased uid
retention. These hemodynamic and neurohormonal changes
result in a hyperdynamic circulation with increased portal
pressures and decreased systemic vascular resistance.
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_38
419
420
R. Koppula and Z. J Haskal
Post-hepatic Portal Hypertension
• Right heart failure
• Tricuspid regurgitation
• Constrictive pericarditis
• IVC obstruction
• Budd-Chiari syndrome
Intrahepatic Portal Hypertension
Fig. 38.1 Classication of portal hypertension
Table 38.1 Clinical complications of cirrhosis with associated porto-
systemic gradient thresholds
Pressure gradient (mmHg) Clinical implication
0–5 Normal portosystemic gradient
10 Development of gastroesophageal varices
12 Esophageal variceal bleeding
16 Increased mortality/clinical
decompensation in patients with varices
>20 Increased risk of failed medical therapy
in acute variceal bleeds
• Cirrhosis
• Schistosomiasis
• Hepatitis
• Veno-occlusive disease
• Sclerosing cholangitis
• Primary biliary cirrhosis
Pre-hepatic Portal Hypertension
• Portal vein thrombosis
• Splenic vein thrombosis
• Splenomegaly
• Mesenteric arteriovenous fistula
• Wilson’s disease
• Hemochromatosis
• Alpha-1 antitrypsin
• Granulomatous disease
• Congenital fibrosis
regulated renal vasoconstriction secondary to decreased
renal blood ow [15].
Initial management of ascites involves treating the under-
lying liver disease, sodium restriction, and the use of oral
diuretics such as spironolactone and furosemide. With worsening disease, patients may become resistant to or intolerant
of diuretic therapy (>400mg/day spironolactone or 160mg/
day furosemide), at which point serial large- volume paracenteses (LVP) are required (refer to Chap. 42 for more information) [16].
Conventional Therapy
Ascites
Ascites is the most common complication of cirrhosis and
portal hypertension. Approximately 58% of patients with
cirrhosis develop ascites within a decade of diagnosis and
usually have a PSG of >12mmHg [13, 14]. Clinically, ascites presents as worsening abdominal distention and discomfort with associated weight gain, shortness of breath, and
early satiety. Ascitic uid can also pass through diaphragmatic pores into the pleural space, leading to hepatic hydrothorax. Progressive metabolic derangement and systemic
hypotension can also lead to hepatorenal syndrome. This
potentially life-threatening form of kidney injury is thought
to be caused by underlying liver disease resulting in dys-
Varices
Portosystemic collaterals develop to decompress the highpressure portal system by diverting blood away from the liver
into the systemic circulation though the left gastric, splenorenal, and other venous pathways. Esophageal and gastric varices are the most clinically signicant given their propensity to
hemorrhage. Ectopic varices can develop within the duodenum, retroperitoneum, abdominal wall, rectum, and bladder
(Fig.38.2).
Esophageal variceal hemorrhage occurs in approximately
25–40% of patients with cirrhosis, with each episode carrying
an approximate 30% mortality risk [17, 18]. Increasing variceal
diameter, intravariceal pressure, and worsening liver disease
are associated with increased risks of hemorrhage [19].
Gastroesophageal
collaterals
Paraumbilical
Left gastric vein
IndicationsContraindications
38 Transjugular Intrahepatic Portosystemic Shunt (TIPS) andPortal Hypertension
collaterals
421
Short gastric
veins
Portal vein
vein
Inferior
vena cava
Umbilicus
Fig. 38.2 Portosystemic collateral circulation seen in portal hypertension
Table 38.2 Indications and
contraindications for TIPS, with
Prevention of secondary variceal hemorrhage
relative strengths of evidence for
each indication
+++
Refractory acute variceal hemorrhage
+++
Refractory ascites
+++
Gastroepiploic
collaterals
Splenorenal
collateral
Splenic v.
Superior
mesenteric v.
Inferior
mesenteric v.
Mesenteric /
retroperitoneal
collaterals
Hemorrhoidal
Severe or rapidly progressive liver failure
Severe hepatic encephalopathy
Severe heart failure
Budd-Chiari syndrome
++
Portal gastropathy
++
Hepatorenal syndrome
++
Hepatopulmonary syndrome
+
= absolute contraindications = relative contraindications.
Portal hypertensive gastropathy differs from variceal bleeding as it usually manifests as slow gastric oozing [20].
Once the presence of high-risk varices is diagnosed on
screening endoscopy, prophylactic treatment consists of
endoscopic variceal ligation (EVL), sclerotherapy, and nonspecic beta blockade. In the setting of acute esophageal variceal hemorrhage, rst-line treatment involves local endoscopic
control of bleeding combined with pharmacologic therapies
such as somatostatin and vasopressin.
Severe pulmonary hypertension
IV contrast allergy/renal insufficiency
Biliary obstruction
Hepatic/pancreatic malignancy
Portal system thrombosis
Interventional Therapy
A TIPS is a percutaneously created portosystemic shunt used
to reduce portal pressures. It is a method of diverting blood
ow from the portal vein directly to the hepatic veins, bypassing the area of increased resistance in the hepatic parenchyma
[21]. Common indications as well as contraindications are
listed in Table38.2 and are discussed below.
422
[]
()
()
()
()
/.
l6
R. Koppula and Z. J Haskal
TIPS is indicated for refractory ascites, with improved
outcomes relative to LVP:
• Improved control of ascites compared to LVP (62%
vs.24%)
• Improved transplant-free survival at 2years compared to
LVP (49% vs. 35%), although the TIPS group demonstrated
increased rates of hepatic encephalopathy [22]
TIPS is indicated for acute variceal hemorrhage if endoscopic therapy fails and for secondary prevention of variceal
bleeding [23].
• In refractory variceal bleeding, TIPS results in cessation
of hemorrhage in approximately 93% of patients [24].
• Compared to EVL and pharmacotherapy, TIPS performed
within 72 h of acute variceal hemorrhage demonstrates
lower rates of re-bleeding (3% vs 45%) and improved
1-year survival (86% vs 61%) [25].
• For recurrent variceal hemorrhage, TIPS results in decreased
rates of re-bleeding (19–21%) compared to endoscopic
therapies (44–52%) [25].
TIPS is contraindicated in patients with severe heart failure
or encephalopathy. Patients with advanced liver disease may
not tolerate diversion of nutrient-rich portal ow away from
the hepatic parenchyma. Severity of liver disease is often categorized using two scoring systems. The Child-TurcottePugh (CTP) (commonly called the Child- Pugh class or score)
incorporates clinical symptoms of encephalopathy and ascites in addition to serum bilirubin, albumin, and international
normalized ratio (INR) to categorize liver disease into class A
(compensated cirrhosis), B, and C (decompensated cirrhosis).
CTP class C (or CTP score>12) is associated with high risk
of early death after TIPS [26].
The Model for End-Stage Liver Disease (MELD) score is
the other prominent scoring system and is calculated in the
following manner [27, 28]:
MELD score bilirubingmdL
∗
+
11 2957
()
INR
.ln.
()
∗
=
378
.ln/
∗∗
+
creatininemgd
[]
+ln
43
• Elective TIPS cases should be avoided in patients with
MELD scores >24 [32].
• Patients with MELD >18 should be informed of the signicant increase in mortality at 3months (35% vs. 16%)
[33].
Key Point
Child-Pugh score>12 and MELD score>25 are associated with a higher mortality rates following TIPS.
Creation of a portosystemic shunt can result in or worsen
hepatic encephalopathy. Increasing age, history of prior
hepatic encephalopathy, and higher CTP scores are associated with increased risks of developing encephalopathy after
TIPS [34]. TIPS also increases cardiac preload and output. In
patients with right/left heart failure or hypervolemia, this may
lead to cardiac decompensation or pulmonary edema.
Therefore, TIPS should be avoided in patients with mean pulmonary artery pressures >45mmHg.
Additional relative contraindications to TIPS increase
the technical difculty of the procedure and are listed in
Table 38.2. However, with experience and proper case
selection, TIPS can be performed successfully in these
scenarios.
Baseline LFTs, CBC, and a coagulation panel should be
drawn to assess for baseline liver disease, anemia, and coagulopathy. Acutely bleeding patients should be stabilized and
properly resuscitated before undergoing TIPS creation. This
may include blood products, cryoprecipitate, fresh frozen
plasma, intravenous pressor support, and balloon tamponade
catheters. Pre-procedure antibiotics are administered.
Imaging (sonography, CT, or MRI) should be performed prior
to the procedure to ensure patency of the hepatic and portal
veins, and to exclude hepatic masses. In patients with a history of heart disease, further work-up with a cardiology consultation and/or echocardiography may be warranted. TIPS
can be performed with conscious sedation or general anesthesia based on physician preferences.
The MELD score has been validated in predicting mortality
and outcomes after TIPS and is also used to determine liver
transplant allocation by the organ procurement and transplantation network (OPTN) [29].
• Studies have shown that patients with MELD scores >25
are associated with higher mortality rates after TIPS
(42%, 65%, 72% at 0, 3, and 6months, respectively) when
compared to low-risk patients (MELD <10) [30, 31].
The How To
1. The right internal jugular vein (IJV) is the most
common site of vascular access for TIPS given the
favorable course to the hepatic veins. The left IJV,
femoral vein, transhepatic, and transcaval routes
have also been used. A guidewire is passed through
the heart into the IVC; it is especially important to
monitor for EKG changes during this step as
(continued)
38 Transjugular Intrahepatic Portosystemic Shunt (TIPS) andPortal Hypertension
arrhythmias can be induced by guidewire manipulation in the right atrium.
extending from the portal vein to the IVC
2. A long 10-French (Fr) vascular sheath is used to
measure baseline pressures. If unanticipated high
tion of diuresis should be considered. In elective
cases, this may warrant a change in treatment plan.
3. A hepatic vein is selected using a 5-Fr diagnostic
curved catheter, usually the right hepatic vein
38.3).
4. Wedged venography is performed. Iodinated or carbon dioxide contrast can be injected during balloon
to their inferior patency rates compared to stent
grafts [26].
8. Repeat pressure measurements and venography are
obtained to determine the post-TIPS portosystemic
gradient, to reassess variceal flow, and to determine
if further shunt dilation is necessary.
9.
using various combinations of coils, sclerosants, or
plugs (see Chap. 39 for more information).
-
tem, creating a guiding map for the creation of the
38.4).
5. The TIPS needle and sheath are advanced from
The goal of the TIPS is to create the smallest caliber shunt
to treat the clinical indication. Common PSG endpoints for
specic indications are discussed below:
within the hepatic vein through liver parenchyma to
the anticipated direction of the intrahepatic portal
vein branch. The needle is withdrawn while applying suction until blood return is visualized within
• Esophageal varices: PSG≤12mmHg. Cases with gastric
varices and a gastrosplenorenal shunt may require smaller
gradients or balloon-occluded retrograde transvenous
obliteration (BRTO) as indicated.
38.5a).
6. A guidewire is quickly passed into the portal vein
38.5b), and splenic and portal venography is
performed. Portal pressures are recorded, allowing
calculation of the portosystemic gradient.
7.
and measured for graft length selection. A polytet-
• Refractory ascites or hepatic hydrothorax: The endpoint
gradient is less well-established. Some interventionalists
believe a lower endpoint gradient is required, approximately ≤8mmHg, while others contend that this unnecessarily increases the risk of hepatic encephalopathy or liver
failure [35]. Current TIPS stent grafts allow progressive
future dilations, which can be performed in an outpatient
setting if the initial result is inadequate.
423
38.5c, d). Bare metal stents are rarely used due
Fig. 38.3 Selection and opacication of the right hepatic vein. (a) The
5-Fr diagnostic catheter (red arrow) is used to select the hepatic vein,
followed by advancement of the long vascular 10-Fr sheath (blue arrow)
into the vein. (b) Contrast is injected through the sheath (blue arrow) to
opacify the hepatic vein (red arrow) to ensure that there is no venous
outow blockage.