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104
I. G. Lupescu and M. C. Grasu
horizontal level between air and cystic uid. CT report:
pointing the CT diagnostic criteria and the exclusion of a
simple liver cyst.
13.2.4 CT inPre-/and Post Liver
Transplantation
Liver transplantation (LT) is the only curative treatment
for acute fulminant and chronic liver disease as well and in
patients with HCC who do not have enough liver function
reserve [5]. Medical imaging plays a major role in performing the pretransplant balance as well as in monitoring of
posttransplant patients [2, 7, 19, 22–25].
CT evaluation of the liver in pretransplant At the
donor, MDCT angiography (MDCTA) provides a com-
plete mapping of liver parenchyma, vascular anatomy
(HA, PV, HV), allowing accuracy measurements of the
liver volume, very important elements for virtual surgical
planning. Knowing these anatomical variants, the surgeon
can elaborate an adequate arterial, venous and biliary
reconstruction plan [2, 7, 19, 20, 24]. At the receiver, CT
imaging allow exclusion of absolute contraindications in
LT: extrahepatic malignancy, inltrating or diffuse hepatic
tumor, extensive venous thrombosis of the PV axis and of
the SMV [2, 7, 20, 25].
CT evaluation of the liver in post-transplant Aspects
encountered early in LT are represented by periportal oedema
(21%), uid collections at the level of the liver hilum; peri-/
subhepatic hematoma; small left pleural uid [25–30].
Vascular complications (VC). MDCTA is the method of
choice; VC are represented by: HA stenosis; HA thrombosis
(Fig. 13.7); HA pseudoaneurysm; stenosis of the inferior
vena cava (IVC), PV stenosis at anastomosis level; thrombosis of PV or IVC [25–31].
Fig. 13.6 Liver abscess: nonenhanced central hypodense area surrounded by a capsule, with a uniform thickness that enhance after CM injection
(black arrow). Note also the perfusion abnormalities adjacent to the abscess and the hemangioma (white arrow).
a
Fig. 13.7 Hepatic artery thrombosis (white arrow) in a patient with liver transplant-MDCTA in axial plane (a) and coronal reconstruction (b)
b
13 CT inHepato-Bilio-Pancreatic Surgical Pathology
105
Biliary complications after LT are evaluated using ultrasound and MRI and are represented by biliary obstruction,
biliary stula, biliary tree lithiasis [3, 31].
Intraparenchymal complications (IPC). The main IPCs are:
liver graft infection, liver infarction, acute and chronic rejection. Malignancies. The most common neoplasms are HCC
recurrence and lymphoproliferative syndromes [32, 33].
13.3 CT inLiver, Biliary Tree andPancreatic
Traumatic Injuries
Liver trauma MDCT is the best imaging modality to evaluate liver trauma. CT aspects. Lacerations appear as irregular
linear/branching areas of hypoattenuation; different grade of
parenchymal disruption; vascular liver injury (arterial, venous)
or active bleeding. Acute hematomas appear as a hyperdense
accumulation compared to normal liver parenchyma located
between the liver and its capsule or can be intraparenchymal
[3, 12]. CT report must contain the complete list of parenchy-
mal and vascular liver injuries and of others associates intrabdominal posttraumatic or nontraumatic lesions.
CT in pancreatic trauma (PT)
PT are represented by: enlargement of the pancreas with
hypodense laceration of the pancreatic parenchyma;
heterogeneous parenchymal enhancement; uid collections
(pseudocyst, abscess or hematoma); pancreatic duct disruption. Secondary signs: peripancreatic fat stranding, uid or
hematoma between the pancreas and splenic vein, peripancreatic uid, thickening of perirenal fascia’s [3, 6].
CT in biliary trauma Gallbladder (GB) injury. CT
aspects. Presence of pericholecystic free uid, intraluminal
or pericholecystic high-density hematoma, or GB wall thickening. Poor denition of GB, GB wall contour abnormal, or
CT aspects. Direct signs of
collapsed GB, particularly with surrounding pericholecystic
uid, raises suspicion for GB perforation. Unusual position
of the GB or separation of GB from the normal location in
cases of avulsion. Bile duct injuries. CT aspects. Free uid
or loculated collection (bilioma) in right upper quadrant
adjacent to biliary tree [3, 7].
13.4 CT inAcquired Biliary Tract Pathology
Primitive sclerosing cholangitis (PSC) is an autoimmune
disease in which the IHBD and EHBD become inamed,
scarred, narrowed or blocked. CT aspects and report: alter-
nation of dilatations and areas of stenosis, appearance of
“winter tree”; lobar atrophy in the affected area; abscesses,
development of liver cirrhosis and portal HT, development of
BD carcinoma [3, 5, 34]. Secondary sclerosing cholangitis.
Occur as a result of chronic bacterial cholangitis secondary
to biliary strictures/choledocholithiasis; by postischemic BD
changes; infectious cholangitis from AIDS; secondary to
congenital bile duct abnormalities; in BD neoplasms; secondary to postoperative changes of the BD [3, 31].
CT aspects and report: BD dilation with inequalities of
calibre, contrast enhancement of the BD walls; hyperdense
biliary lithiasis [3, 5, 31].
Biliary tree lithiasis
terol (70%): transparent (93%), calcied (7%); discreetly
hypodense compare to the biliary uid; pure cholesterol
stones (transparencies); small stones (cholesterol + bilirubin
+ calcium)—spontaneous hyperdense in CT.Location: intrahepatic lithiasis, extrahepatic BD, in the gallbladder, in the
cystic duct [3, 5]. CT aspects: gallstones are visible in
60–70% of cases. CT report: location, appearance, size of
the stone(s), signs of obstruction, complications (Fig.13.8),
associated lesions [3, 5, 7, 8].
Composition of gallstones: choles-
Fig. 13.8 Calcied biliary lithiasis involving the CHD and the choledoc (white arrow) and liver abscess (black arrow)
106
I. G. Lupescu and M. C. Grasu
Acute cholecystitis (AC). CT aspects: GB distention; GB
wall over 3mm thick, hyperdense; mucosal hyperenhancement;
densied gallbladder (GB) content; pericolecistic fat stranding
or uid; changes in hepatic perfusion in the early AP, with transient enhancement in the pericolecistic liver parenchyma.
Complications: emphysematous cholecystitis (hypertransparent air accumulations in the GB projection area);
pericolecistic abscess; Mirizzi syndrome; gangrene;
Bouveret’s syndrome (calculus that eroded the GB wall,
migrated into the duodenal lumen with obstruction); biliary
ileus: migration of the GB stone in the gastrointestinal tract
secondary to bilio-digestive stula and inclusion in the narrowing areas of the digestive tract: Treitz angle, ileocecal
valve, sigmoid colon, characterised by diagnostic triad:
occlusive syndrome, aerobilia and hyperdense lithiasis [3,
6–8]. Gangrenous cholecystitis: occurs in immunocompro-
mised patients; evolves into parietal necrosis and perforation; vesicular perforation can be done intraperitoneally, in
the digestive tract (duodenum, colon) or can be collected in
the GB bed in the form of a perivesicular abscess [3, 6]. CT
report: calculus embedded in the cystic duct, pericholecystic inammatory changes, complications, exclusion of
acute pancreatitis or of a perforated duodenal ulcer.
Chronic cholecystitis is a chronic inammation of the GB
walls. The causes of chronic cholecystitis are GB stones and
cystic duct obstruction; the GB wall is increased in thickness
(average 5mm), with regular or irregular contour. Particular
forms. Xanthogranulomatous cholecystitis is part of the
chronic inammations of the GB, simulating both clinically
and imagistically a GB carcinoma [3, 7, 8]. The porcelain
bladder represents the deposition of calcium carbonate in the
GB wall; associated with GB stones in 90% of cases [3].
CT aspects and report: parietal GB changes associated
with density content changes (hyperdense content in porcelain GB), exclusion of a GB carcinoma [3, 7, 8].
13.4.1 Biliary Tree Tumors
Cholangiocarcinoma (CC). CC are malignant tumors originating in the BD epithelium with peripheral (intrahepatic),
centrohilar topography (Klatskin tumor) or located at the
extrahepatic BD (EHBD) level: common hepatic duct (CHD)
or choledochus. Intrahepatic CC represents approximately
20% of all CC, being the second most common liver tumor
after HCC.In the Klatskin tumors or in tumors of EHBD level,
there are the following forms: obstructive with amputation in
U or V (70–85%); stenotic (10–25%) with irregular edges
appearance; polypoid (5–6%), with upstream BD dilation. The
incidence of Klatskin’s tumor represents 70% of CC cases.
Lymphatic extension (48%), inltration in the liver parenchyma (23%); peritoneal determinations (9%); hematogenous
disseminations are rare (liver, lung, peritoneum).
CT aspects. Intrahepatic CC: focal or segmental dilation
of IHBD (see Fig.13.4); segmental BD stenosis or presence
of endoluminal polypoid mass [35]; spontaneous hypodense
mass; after CM i.v. injection the tumor demonstrate heterogeneous peripheral enhancement with gradual centripetal
enhancement. The rate and extent of enhancement depend on
the degree of central brosis; segmental atrophy may be
associated; portal invasion is rare [2, 3, 5–8, 36, 37]. Central
CC: IHBD dilation, without distal EHBD dilation. Staging
of the central CC (Bismuth and Corlette classication). Type
I: tumor at CHD level with respect of the bifurcation. Type
II: the tumor inltrates CHD extending to the bifurcation.
Type III a: inltration of the CHD, bifurcation with right BD
extension and right second-order branches involvements.
Type III b: inltration of the CHD, bifurcation, left hepatic
duct, and left second-order BD branches. Type IV: tumor at
the level of CHD, R and LCHD and of the second order BD
branches [2, 3, 5–8, 36, 37]. CC at CHD level: mass circum-
scribing the CHD, inltrative or polypoid type (Fig.13.9),
Fig. 13.9 Central cholangiocarcinoma-polypoid type (white arrow) involving the CHD and the bifurcation with symmetrical IHBD dilatation
(black arrow)
13 CT inHepato-Bilio-Pancreatic Surgical Pathology
107
with upstream BD dilatation. Choledochal CC: more frequently inltrative lesion, rarely polypoid lesion. Dilation of
the GB, CHD and IHBD are associated [2, 3, 5–8, 36, 37].
CT report: correct and complete evaluation of the tumor,
resectability criteria, exclusion of benign BT pathologies,
associated lesions [12].
Gallbladder carcinoma Represents the fth tumor, in frequency, from malignant tumors of the gastrointestinal tract [5,
6]. There are two forms of GB neoplasm: nodular and inltra-
tive with localized or diffuse thickening of the wall, difcult
to differentiate from a scleroatrophic GB.The extension is
made quickly towards the hilum, the hepatic pedicle and into
the hepatic parenchyma (in the V, VI or IV liver segments).
Regional lymphadenopathies may be present in the hepatic
and peripancreatic pedicles. The mechanisms of EHBD
involvement are represented by direct contiguous invasion or
compression on CHD or choledocus, given by lymphadenopathies or by the tumor mass itself [2, 3, 5–8, 36, 37].
13.5 CT inPancreatic Pathology
Acute pancreatitis (AP) represents the acute inammation
of the pancreatic tissue that causes changes in structure and
function [1, 5, 6].
CT aspects and report. The Balthazar classication groups
5 stages: A and B correspond to the oedematous form of AP;
stage C corresponds to AC that associates peripancreatic
inammation; stages D and E correspond to extensive complicated AC with poorly dened-phlegmon-type collections.
CT visualizes the pancreas in 98% of cases. CT scan high-
light: diffuse increasement with convex edges of the pancreas;
hypodense/or absence of enhancement of the pancreatic tissue in necrotic areas; peripancreatic fat inltration; thickening of the perirenal fascia’s; hyperdense areas (50–70UH) in
hemorrhagic AP; intra-/peripancreatic uid collections
(Fig.13.10); identication of uid collection, pseudocyst (s)
or of abscesses; assess the opportunity and the optimal
approaches in the post AC encysted collections [1, 3, 5–8].
Chronic pancreatitis (CP) is a persistent and progressive
inammation of the pancreatic tissue that leads to irreversible alterations in anatomical architecture and pancreatic
function. There are several types of CP: calcied, obstructive, autoimmune, pseudotumoral, groove pancreatitis [1, 3,
5, 6]. CT aspects and report: moniliform dilatation of
Wirsung duct (WD); intrapancreatic, intraductal calcications (CT +++); atrophic appearance of pancreatic tissue;
intra-/peripancreatic pseudocyst, focal/diffuse enlargement
of the pancreas; moderate dilation of choledoc; others
lesions: splenomegaly; splenic vein thrombosis; formation
of arterial pseudoaneurysms; thickening of the peripancreatic fascia [1, 3, 5, 6, 12, 38, 39].
Pancreatic pseudocyst is an encapsulated uid collection delimited by brous tissue with dimensions generally
between 2–10cm. Location: 2/3 are located in the pancreas;
atypical topography: intraperitoneal, retroperitoneal, subcapsular (hepatic, splenic, renal), mediastinal, in the cervical
region. It can communicate with the stomach, duodenum,
spleen [1, 3, 5–8, 12].
CT aspects and report: uid/parauid density (0–30 UH)
collection with well delineated wall, extremely rare parietal
calcications; changes in peripancreatic fat. Complications:
rupture, hemorrhage, infection, intestinal obstruction [1, 3,
5–8, 12].
Fig. 13.10 Acute pancreatitis with necrotic areas (white arrow) and multiple peripancreatic uid collections (dotted arrow)
108
I. G. Lupescu and M. C. Grasu
13.5.1 Pancreatic Tumors
Serous cystadenoma represents 50% of all pancreatic cystic
tumors and 1–2% of exocrine tumors of the pancreas; may be
associated with von Hippel Lindau syndrome [1, 5, 6].
CT aspect: honeycomb cystic areas; after contrast, the
septa and the periphery enhance; characteristic: central
brous scar sometimes calcied.
Mucinous cystadenoma/cystadenocarcinoma corresponds to a single cystic or multiloculated mass, delimited
by a thick wall, sometimes with dense nodules on the internal contour, containing mucin in the cystic areas [1, 3, 5–8,
12]. CT aspect: intratumoral septa; uid densities into the
cysts; the tumor is generally hypovascular; positive enhancement of the walls and septa of the cysts; calcications. Liver
metastases are cystic, round with a regular thick wall.
Intraductal papillary mucinous neoplasm (IPMN) represent a mucinous ductal ectasia, with malignant potential.
The location is in the WD causing global or focal dilation, or
in the afferent branches [3, 6, 12]. CT aspects and report.
Cystic dilatation of WD and related branches; presence of
mural nodules and thick septa in malignant lesions; pancreatic tissue atrophy [3, 6, 12, 40].
Pseudopapillary solid tumor is a cystic and solid tumor
with a low degree of malignancy [3, 7, 8, 12]. CT aspect:
heterogeneous mass with important contrast uptake in the
venous phase (Fig.13.11); presence of calcications in 30%
of cases.
Pancreatic ductal adenocarcinoma (PDAC) is the most
common malignancy of the pancreas. 65% of cases are invasive tumors which presents at the time of diagnosis distant
metastases. 21% of cases have lymph node invasion. Only
14% have a tumor located strictly into the pancreas. CT
aspects: pancreatic mass (95%), diffuse enlargement (4%),
normal appearance (1%); hypodense, hypovascularized;
dilation of choledoc and WD without noticeable tumor mass
(4%); dilatation of EBD and IHBD (38%), dilatation of WD
(67%); pancreatic body and tail atrophy of (20%); pseudocyst (11%); calcications (2%); arterial and venous invasion
(Fig.13.12); invasion of lymphatics; venous collateral circulation; thickening of the Gerota fascia; posterior tumor
extension; extension to the splenic hilum and hepatic hilum;
contiguous invasion of adjacent organs (duodenum, stomach, root of the mesentery).
CT report: 1. establishing resectability criteria: no contact
with the celiac axis (CA), SMA, or common hepatic artery.
Vein: no contact or abutment to the SMV or PV. 2. unresect-
able locally advanced-see Fig. 13.12). Artery: encasement
(tumor–vascular contact>180°) of the SMA, HA or CA, abutment or encasement of the rst jejunal SMA branch, or abutment of the CA and aortic involvement. Vein: occlusion or
tumor thrombosis of SMV or PV or abutment or encasement
of the rst jejunal SMV branch; unresectable metastatic-distant metastasis including nonregional lymph node metastasis.
3. borderline resectable: abutment (tumor–vascular con-
tact<180°) or short encasement of the common HA without
extension to the CA or HA bifurcation or abutment of the
SMA or variant artery; abutment or encasement of the CA
without involvement of the aorta, GDA, and SMA. Vein:
abutment, impingement, short encasement of the SMV or PV,
or short segment venous occlusion [1, 3, 5–8, 12, 41–47].
Pancreatic endocrine tumors Pancreatic neuroendocrine tumors are rare tumors that produce hormonal secre-
tion with specic symptoms; the most common are
insulinomas and gastrinomas. Associated with MEN I syndrome; von Hippel Lindau disease, neurobromatosis and
tuberous sclerosis. The degree of malignancy is variable [1,
3, 5–8, 12]. CT aspects. Frequently are tumors with a diam-
eter of less than 3cm, hypervascularized; bulky tumors have
necrotic and hemorrhagic areas; In most cases there are no
signs of WD obstruction. CT aspect: location, number, semiological appearance of the tumor/tumors, signs of malignant
degeneration, distant metastases.
Pancreatic non-secreting endocrine tumors are often
larger than secretory neuroendocrine tumors; 80% of tumors
are hypervascularized; 20% are hypovascularized; cystic/
Fig. 13.11 Pseudopapillary solid tumor-large heterogenous pancreatic mass with cystic and solid areas (white arrow)
13 CT inHepato-Bilio-Pancreatic Surgical Pathology
109
Fig. 13.12 Invasive pancreatic adenocarcinoma: cephalo-isthmic pancreatic mass (white arrow) with invasion of celiac axis, HA, SMV and PV
necrotic components are common; bulky tumors may have
calcications; tumors over 5 cm are frequently malignant
and can cause WD obstruction and dilation [1, 5, 6].
CT aspects: intense enhancement in 80% of cases; bulky
tumors are heterogeneous with necrotic areas and calcications. CT report: location, number, semiological appearance
of the tumor/tumors, signs of malignant degeneration, distant metastases.
Pancreatic metastases occur in the terminal stages of a
primary tumor, more commonly in renal cell carcinoma.
in early postoperative period in case of fever, leukocytosis,
abdominal pain, jaundice or suspicion of bleeding or peritonitis. Early complications include collections, vascular
thromboses, biliary, pancreatic or vascular injuries. Late
complications are related mainly to the initial disease relapse.
MDCT protocol include a nonenhanced phase (to detect
hyperdense collection like hematoma), an AP to assess active
bleedings and a PVP to detect and characterize complications like liver abscesses or venous thromboses (portal,
mesenteric).
Primary tumors: renal, lung, breast, colon carcinoma, melanoma, soft tissue sarcoma [1, 3, 5–8, 12]. CT aspects: nodules
with heterogeneous appearance (60%), homogeneous (17%),
iso-/hypodense; hypo-/hypervascularised [1, 3, 5–8, 12].
Liver injuries Pneumobilia, periportal edema and soft-
tissue stranding can be normal ndings during the early post-
operative period in patients with HBP surgery. Transient
uid collections are often seen after HBP surgery and drain-
age is not required, unless clinically indicated. CT aspects.
13.6 CT ofPostoperative Complications
inHBP Surgery
Fluid collections are commonly represented by seromas,
hematomas, bilioma, pancreatic stula or abscesses
(Fig. 13.13). MDCT is more accurate than ultrasound for
Postoperative complications in HBP surgery are not uncommon, due to high complexity of surgical procedures. MDCT
is the most effective postoperative imaging procedure used
diagnosis and characterization of complex collection and is
used to perform invasive procedure if necessary. CT allows
assessment of the size, location and content of the collection.
110
Fig. 13.13 Heterogenous encapsulated collection with multiple aeric bubbles, suggestive for abscess (white arrow). Small right pleural uid (dot-
ted arrow)
I. G. Lupescu and M. C. Grasu
The diagnostic should be correlated with clinical status, laboratory values and surgical procedure. CT-guided procedures
(puncture with aspiration, percutaneous drainage) are often
required for diagnostic conrmation. Hematomas are hyperdense (attenuation between 50–70 HU) on NECT and may
show extravasations of CM when active bleeding is present.
Fluid collections related with leakages from biliary or pancreatic stula have lower attenuation (10–20 HU) and located
near biliary or pancreatic anastomosis. Biliomas are commonly located in the upper right quadrant and appears on
MDCT as a well-dened uid collection, rounded or oval
shaped. Complicated bilioma with hemorrhage or infection
may have attenuation higher than 20 HU.Collections with
gas bubbles and wall enhancement are highly suggestive for
abscesses (see Fig.13.13). Typical aspect on MDCT of an
abscess is a well-dened, rounded hypodense mass, with gas
bubbles inside (in <20% of cases) and wall enhancement
after administration of intravenous contrast.
Vascular injuries and thromboses Postoperative vascular
thromboses may include PV, SV, HV, HA, SMA.Vascular
thrombosis following HBP surgery are rare. MDCTA is used
for a precise evaluation of the vascular tree. CT aspects. A
thrombus typically appears as a nonenhancing lling defect
within the lumen of the vessel, an acute thrombus is hyperdense on NECT.MDCT may document associated signs like
ischemia of the small bowel or perfusion abnormalities of
the liver.
Biliary injuries The post-cholecystectomy BD injuries
may be caused by mistakenly placed clips generating stenosis of the CHD or erroneous section of BD. CT aspects.
MDCT with contrast visualizes the uid collections and dila-
tation of the biliary tract and may detect the level of lesion
and the associate vascular damage (arterio-venous stula,
vasculo-biliary stula) if exists.
Pancreatic injuries The most common complications of
pancreatic surgery are pancreatic stula (related to the WD
damage), abdominal abscesses, intraabdominal bleeding and
anastomotic leakage producing peritonitis and pancreatitis of
the remanent gland. CT aspect. Pancreatic stula is the most
common complication after the partial pancreatectomy. The
most important CT nding is the presence of persistent peri-
anastomotic collection, sometimes with gas bubbles
included.
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Magnetic Resonance Elastography
(MRE) toAssess Hepatic Fibrosis
AliyaQayyum
14
Abstract
Chronic liver disease and cirrhosis are a major worldwide
health problem and represent the 11th leading cause of
death in the USA based on data from 1999 to 2018 [1].
There are many etiologies of chronic liver disease including hepatotoxic factors such as viral hepatitis B and C,
alcohol, nonalcoholic fatty liver disease, hemochromatosis, and autoimmune hepatitis, as well as biliary factors
(toxicities) such as primary sclerosing cholangitis and primary biliary cirrhosis. While liver biopsy is the standard
of reference for diagnosis and monitoring of liver brosis,
it is an invasive procedure associated with a non-negligible complication risk [2]. Bleeding occurs in ~1 of 500
liver biopsies, which may be severe in 1 of 2500 to 10,000
liver biopsies [3]. Additional important complications
include sepsis, pneumothorax, and hemothorax. The
reported mortality risk from liver biopsy is up to 0.3% [4].
Aside from complications, liver biopsy is not an accurate
reference standard. Important limitations of liver biopsy
include small sample size (~1/50,000 part of liver) resulting in sampling errors due to the heterogeneity of diffuse
liver disease, and high intra- and inter- observer variability
in interpretation [5–12].
Cross-sectional imaging with ultrasound, CT, and MRI can
depict morphologic changes that can be present in some but
not all patients with cirrhosis but liver morphology usually is
normal with earlier stages of brosis. MR elastography
(MRE) is an non-invasive technique for quantitatively assessing the stiffness of tissue and is now deployed on more than
A. Qayyum (*)
MD Anderson Cancer Center, Houston, TX, USA
e-mail: AQayyum@mdanderson.org
1500 MRI systems around the world. MRE is often included
as part of a standard liver MRI for evaluation of chronic liver
disease. The normal liver is a soft organ with structural support mainly from the extracellular matrix of the parenchyma,
which is comprised largely of collagen and a thin connective
tissue capsule. In chronic liver injury, activation of the
hepatic stellate cells to myobroblasts results in brosis. The
brosis is associated with alteration of liver blood ow. Both
of these factors contribute to an increase in liver stiffness.
Additional pathological processes that can contribute to liver
stiffness include venous congestion, biliary obstruction, and
inammation within the liver [13]. The premise for clinical
MRE is based on the altered mechanical properties of diseased tissues. The most successful application of MRE to
date is in the detection and staging of liver brosis, which
has driven the use of MRE over the last decade. A normal
liver typically has a stiffness of approximately 2kPa (similar
to subcutaneous fat), whereas a cirrhotic liver may have a
stiffness value of >5kPa. Shear waves propagating in tissues
with higher stiffness will have a greater wavelength and a
faster speed. The basis of MRE exploits the faster propagation of shear waves in stiffer tissue and slower propagation in
softer tissue. During MRE, applied vibration to the organ of
interest is synchronized with a modied phase-contrast MRI
pulse sequence used to image the propagating shear waves.
MRE measures the speed of the propagating shear waves.
The MRE data is used to generate an “elastogram” which is
a grayscale or color “stiffness” map (i.e., magnitude of the
tissue shear modulus in kilopascals/kPa, commonly known
as “shear stiffness” or simply “stiffness”). Liver stiffness is
independent of magnetic eld strength and MRE can be performed on either 1.5T or 3T clinical scanners. However, it is
necessary to perform liver MRE at the same frequency of
vibration to achieve comparable measurements (stiffness
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2022
M. Makuuchi et al. (eds.), The IASGO Textbook of Multi-Disciplinary Management of Hepato-Pancreato-Biliary Diseases,
https://doi.org/10.1007/978-981-19-0063-1_14
113
114
ab
A. Qayyum
depends on frequency). Reportedly, a well-performed liver
MRE study should “achieve a 95% condence interval for a
true change in stiffness when there is a measured change in
hepatic stiffness of 19% or larger” [13–16]. The diagnostic
accuracy of MRE (0.994 for brosis stage >2, 0.985 for
brosis stage >3, and 0.998 for brosis stage >4) is reported
to be greater than that of other tests such as transient elastography (TE), serum aspartate aminotransferase to platelets
ratio index (APRI), and the combination of TE with APRI
[16].
14.1 MRE Technique
There are three key components to MRE: (1) transducers, (2)
pulse sequences for data acquisition, and (3) postprocessing
for converting raw images into an elastogram or stiffness
map. The transducer generates and transmits mechanical
waves into an organ of interest in the body (e.g., liver). All
current commercially available MRE systems use an “active
driver” located outside the magnet room to generate the low
frequency pressure waves. These waves are transmitted by a
coupling tube to a small drum-like device (“passive driver”)
placed on the chest wall overlying the liver (Fig.14.1). The
passive driver converts the pressure waves into vibrations in
the chest wall which generate shear waves in the liver.
MRE is based on a phase-contrast pulse sequence, with
superimposed cyclic motion encoding gradients synchronized with the mechanical waves from the transducer. An
MRE pulse sequence can be either 2-dimensional (2D) or
3-dimensional (3D). A typical MRE sequence involves a
modied 2D echo-planar (EPI) imaging (TR/TE 600ms/min
full (~554.4); slice/gap 8/2mm; ip angle default (90); eld
of view 42cm; matrix 64×64; bandwidth 250kHz; number
of excitations (NEX) 2; 4–6 slices acquired through largest
portion of the liver) (Fig. 14.1). The acquisition time is
16–19seconds (I breath-hold).
MRE postprocessing involves the following steps: (1)
converting the raw phase data into displacement; (2) generating shear-wave images by removing the compressive wave
component; (3) generating wave speed from the shear waves
at the different phase offsets, and (4) generating the elastogram from the wave speed with an inversion algorithm (measurement units in kilopascals, kPa). The standard MRE
Fig. 14.1 (a) The passive driver (blue circle) is placed on the right
lower chest wall overlying the liver. The vertical center of the driver is
in line with the right mid-clavicle (red arrow). The horizontal level of
the driver (black arrows) is in line with the tip of the xiphisternum
(green arrow). (b) MRE images are acquired as 4–6 slices (8mm slices
with 2mm gap) at the level of the widest extent of the liver (blue lines),
while avoiding the liver dome and inferior liver tip