Quick review of hepatobiliary and pancreatic lesion

QUICK REVIEW OF HEPATOBILIARY AND
PANCREATIC LESIONS: SOME LEARNING
POINTS TO SHARE
DR. VINCENT BATISTA LEMAIRE
LOCUM CONSULTANT RADIOLOGIST
SAINT RICHARD ‘S HOSPITAL
WESTERNSUSSEX HOSPITAL NHS FUNDATIONT TRUST
CHICHESTER, WEST SUSSEX, ENGLAND , UK .

THANKS TO PHARMATECH: THREE CONSECUTIVE
YEARS SUPPORTING THE ACTIVITY

QUICK REVIEW OF
HEPATOBILIARY AND
PANCREATIC LESIONS
SOME LEARNING
POINTS TO SHARE

LIVER : BLOOD SUPPLY
1. The normal liver get 80% of blood supply from the portal vein and 20 %
from the hepatic artery .
2. 100% of liver tumours get supply from hepatic artery ; hence will
enhance in the arterial phase .
3. In the portal phase the liver is homogeneous and the hypovascular
tumors is hypodense .

LIVER : TIMING
1. Arterial phase 35 sec. (late arterial ) flow rate 5cc /sec
2. Portal phase : 35-75 sec
3. Equilibrium phase 3-10 min: tumoral wash-out , retention of contrast in
haemangioma ; late enhancement of fibrous tissue in FNH, FLHCC ,
HCC capsule , and the core of cholangiocarcinoma and mets.

GADOXETIC ACID : PRIMOVIST
WHICH TISSUES ENHANCE IN THE LATE HEPATOBILIARY PHASE ?
1. Functional Hepatocytes : FNH
2. Core desmoplastic reaction in metastasis
3. Type 3 inflammatory adenoma: making difficult to differentiate from
FNH
4. The capsule in inflammatory pseudotumor
5. Central fibrosis/desmoplastic reaction in cholangiocarcinoma
6. In cirrhotic patients: macro-regenerative nodules ; low grade dysplastic
nodules ; well differentiated HCC and poorly differentiated HCC with
marked bile production .

GADOXETIC ACID : PRIMOVIST (BAYER) EOVIST (US): GADOLINIUM(GD)-
ETHOXIBENZYL(EOB)-DIETHYLENETRIAMINE PENTAACETIC ACID(DTPA)
1. Hepatobiliary specific agent.: water soluble with a lipophilic EOB group
is attached to gadolinium. Due to the presence of lipophilic EOB group ,
is actively transported from the sinusoidal space into hepatocytes via
organic anion transportation polypeptides .
2. The hepatobiliary phase must be scanned 20 minutes after injection .
3. Basic principle : primary and secondary malignancy do not contain
functional hepatocytes with the ability to take this contrast .
4. The FNH is not a real tumour and shows arterial enhancement that
continues and prolong to the hepatobiliary phase as hyperintense
lesion in a background with lower signal. FNH has functional
hepatocytes with abnormal bile ducts.
5. A potential pitfall using gadoxetic is related to the fast hepatocellular
phase uptake which begins as early as the portal-venous phase.
Therefore , the enhancement of normal liver parenchyma may obscure
the enhancement pattern of the nodule and cause misinterpretation
during dynamic MRI evaluation .

GADOXETIC ACID : PRIMOVIST (BAYER) EOVIST (US): GADOLINIUM(GD)-
ETHOXIBENZYL(EOB)-DIETHYLENETRIAMINE PENTAACETIC ACID(DTPA
Extracellular agents (gadolinium) vs hepatocyte specific agents (Gd-
EOB-DTPA)
1. Arterial phase enhancement similar in timing , less intense with Gd-
EOB-DTPA and possible truncation artefacts.
2. Gd-EOB-DTPA uptake begins almost immediately, leading to progressive
liver enhancement. Consequently there is no pure or equilibrium phase.
The haemangiomas , which remains hyperintense in all phases with
extra-cellular agents, appear to “wash-out” with Gd-EOB-DTPA and after
5-10 minutes become hypointense .
3.The degree of hepatocellular enhancement depends on liver function .

DESCRIBING A LIVER LESION
Characterisation of liver masses
 Hypervascular lesions
 Hypovascular lesions
 Scar
 Capsule
 Calcifications
 Fat
 Hemorrhage
 Cystic components
 Retraction of liver capsule
 Peripheral enhancement and progressive fill in
Publicationdate July 15, 2006This article is based on a presentation given by Richard
Baron and adapted for the Radiology Assistant by Robin Smithuis.
Richard Baron is Chair of Radiology at the University of

LIVER : FINDINGS
1. TSTC : to small to characterise
- In normal background
- If there is a primary malignancy a solitary lesion is usually benign but
needs f/u
- breast carcinoma
2. Hypervascular lesions :
2.0 . varices
2.1 , Haemangioma: with less than 1 cm there is immediate enhancement .
“flash filling .
2.2. FNH : FNH is not a tumor , contains normal hepatocyes . There is
capillary blush which is less dense than the haemangioma in the arterial phase
and isodense with the liver parenchyma in the portal venous and delayed phase.

LIVER : FINDINGS
2.3. Adenoma : capillary blush
2.4. Fibrolamellar HCC : similar to FNH but could have calcification and
the enhancement persist through the venous porta and delayed phase
2.5. HCC : capillary blush . “Every hypervascular mass in a liver with
cirrhosis is a HCC until proven otherwise “.
2.6. Hypervascular mets: capillary blush in mets from breast, renal,
thyroid , carcinoid and sarcomas .

LIVER: FINDINGS
3. Hypovascular lesions :
- cyst
- focal fatty sparing : rounded lesion , does not enhance, fat suppress ,
barely visible on t2 haste .
- focal fatty infiltration in S4: 3rd inflow in S4 , sometimes from aberrant
gastroduodenal artery .
- 10% of HCC
- cholangiocarcinoma
- metastasis: colon , lung , prostate, gastric and TCC
- abscess

LIVER: FINDINGS
4. Capsule :
- abscess
- HCC
- adenoma : thin
- cystadenoma
- cystadenocarcinoma

LIVER : FINDINGS
5. CALCIFICATIONS :
-Mets CRC
- fibro lamellar HCC
- haemangioma
6. FAT :
- adenoma
- dysplastic nodules and HCC
- AML
- metastastic liposarcoma

LIVER: FINDINGS
7. HAEMORRHAGE :
- adenoma
- HCC
- trauma
8. Cyst
- simple - cystic mets
- traumatic - abscess
- biloma - focal liver sparing
- Caroli ‘s disease - echinococcosis
- biliary cystadenoma -

LIVER: FINDINGS
9. Capsular retraction
- metastasis ( pseudo-cirrhosis )
- portal vein thrombosis
- confluent hepatic fibrosis : wedge shaped with overlying hepatic
capsular retraction : t1 hypo , t2 hyper, hypo enhancing lesion with
uniform hyper enhancement in the delayed phase . Usually involved the
medial segment of the left lobe or anterior segment of the right lobe .
The inflammatory component shows high signal on arterial phase and
the fibrous tissue high signal on hepatobiliary phase.

LIVER INCIDENTALOMAS
Benign or Significant Significant
UDO (Unidenetified simple cyst, biliary Multiple TSTC in a
dark objects ) hamartomas , focal fat, TSTC patient with cancer
(to small to characterize)
UBO ( Unidentified Haemangiomas , FNH adenomas (>5 cms)
Bright objects)
UTBO ( Unidentified THAD/THID THAD/THID
transient bright objects) Transient hepatic attenuation associated with mass
differences/intensity differences
Maarten Van Leeuwen

CYSTIC LESIONS OF THE LIVER
I. Simple cyst
1. Benign developmental hepatic cyst
2.von Meyerburg complex
3. Caroli Disease
4. Adult polycystic disease
II. Complex cyst: with one or more features : wall thickening or irregularity, septation
,internal nodularity , enhancement , calcification and haemorrhagic or
proteinaceous contents,
Neoplasm:
Biliary cystadenoma or cystadenocarcinoma
Cystic metastasis
Hepatocellular carcinoma
Cavernous hemangioma
Embryonal sarcoma

CYSTIC LESIONS OF THE LIVER
Inflammatory or infectious
Abscess
Pyogenic
Amebic
Echinococcal cyst
Postraumatic and miscellaneous
Pseudocyst
Hematoma
Biloma
Infected or hemorrhagic cyst

POLYCYSTIC LIVER : INTRACYSTIC
HAEMORRHAGE

LESIONS OF THE LIVER
1. FOCAL FATTY SPARING : usually geographic near the gallbladder fossa and porta
in a background of fatty liver . Hypoechoic on US ; hyperdense on CT ,
Hyperintense on out-phase where the fatty liver shows signal drop .
2. FOCAL FATTY DEPOSITION : medial aspect of left lobe, along the falciform
ligament , gallbladder fossa and central aspect of segment IV near the portal vein .
Sometimes secondary to inflow in S4 from aberrant gastroduodenal artery
.Hyperechoic on US , hypodense on CT and signal drop on out phase .
3. MULTONODULAR HEPATIC STEATOSIS : multiple hyperechoic nodules on US non
visible on MRI T2 but on GRE chemical shift with drop in signal .
4. SOLITARY NECROTIC NODULE OF THE LIVER: h/o trauma , alcohol abuse.
Lobulated well-defined lesion that does not enhance; sub-capsular location ;
could show a subtle rim of enhancement due to inflammatory infiltrate. DD with
mets, lymphoma, pseudotumor.

FATTY DEPOSITION
2 years later

NUTMEG PATTERN, ABNORMAL PERFUSION
(GD-EOB-DTPA)

NUTMEG PATTER: PERFUSION ABNORMALITY :
GD-EOB-DTPA

5 . HAEMANGIOMA : most frequent lesion apart of the simple cyst .Small
haemangioma can present as “flash-filling “ lesions only seen in the arterial phase.
Usually hyperechoic with no significant flow on Doppler but could be “atypical “ and
hypoechoic with peripheral flow . On CT hypodense , on MRI t1 hypo and t2 hyper . On
CT and MRI dynamic contrast enhancement : peripheral discontinuous nodular
enhancement with progressive filling-in (wash-in) and homogeneous in late phases
(12 minutes).
SCLEROSING HAEMANGIOMA : atypical signal , few cases published , can be
differentiated from tumor through biopsy
6. FOCAL NODULAR HYPERPLASIA : second most common “tumor” , most
frequent is woman, formed by aggregates of hepatocytes secondary to an
underlying vascular malformation . The Kupffer cells are present . The “central
scar “ is not a true scar : are blood vessels, bile ducts and sometimes are of
fibrosis . Usually isoechoic or hypoechoic. On CT and MRI arterial enhancement
and wash-out ; the scar t2 hyperintense due to vascular channels ; MRI specific
agent Gd-EOB-DTPA: homogeneous or heterogeneous enhancement in the
hepatocellular phase and reticulation lace –like appearances. The central scar low
signal early phase and becomes hyperintense on late phase..

8. ADENOMA: relatively rare ; female patient ; well circumscribed contain
well-differentiated hepatocytes lacking bile ducts or portal tract with a
variable amount of haemorrhage , fat , necrosis or very rare,
calcification . Hypoechoic on US ; moderate enhancement on arterial
phase . There is no accumulation of hepatospecific agent on
hepatobiliary phase . Type 1, rich in fat , shows drop in signal in out-
phase; Type 2 , catherine mutated Ha-HCC in obese patient , does not
uptake PRIMOVIST ; Type3, inflammatory , formerly called
telangiectatic can show liver uptake in the hepatobiliary phase .Late
rim enahncement,
9. HAMARTOMA/ ANGIOMYOLIPOMA; formed by smooth muscle, adipose
tissue and vessels: mixed (+ common ) ; lipomatous (>70% fat) ,
myomatous (,10% fat ) and angiomatous . Hyperinetnse ON Haste , loss
of signal in out phase imaging , no restricted diffusion , show
centripetal enhancement but hypointense on hepatobiliary phase ; may
have peripheral enhancement simulating mets, but mets have a
dysplastic core which enhance in latera phase giving target appearance
.

10. ABSCESS: presents as a complex cyst ; three layers; the differential
between abscess and mets: mets low adc>abscess ; core
enhancement late phase, nodularity vs septation .
11. NEUROENDOCRINE METS: intense arterial enhancement and wash-
out . Note that only 2 of 3 malignant lesions show wash-out : sensitivity
70%
12. LYMPHOMA: infiltrating , t1 hypo, t2 hyper, high on DWI with low ADC .
Very rare , could be associated to EBV

13. INFLAMMATORY PSEUDOTUMOR : fever, malaise , weight loss, abdominal
pain . On T2 central hyperintense core (most of the lesions are isointense);
peripheral enhancement , septa . Late capsular enhancement due to the
presence of inflammatory cells and coagulative necrosis . DD with
granulomatous disease TB and sarcoid only by biopsy .
14. HYPERESOSINOPHILIC SYNDROME : fatigue , weight loss, fever, 56%
eosinophils .Eosinophil-related tissue damage (parasitic infections , allergic
reactions , hypereosinophilic syndome and tumors). Hypoechoic on US with ill-
defined margins; Hypodense on CT ; t1 iso /hypo , t2 iso/hyper . There are
branches of the portal vein through a subcapsular wedge- shaped ,irregular
lesion
15. FIBROLLAMELAR HCC : young adults ; large , well-defined with low T1 , with
early enhancement and wash-out and a central radiating scar in 80 % of cases
that remains hypointense in all phases a difference of the FNH

HAEMANGIOMAS
No contrast arterial
Portal V Equilibrium

SCLEROSING HAEMANGIOMA GD-EOB-DTPA

SCLEROSING HAEMANGIOMA GAD 15 MONTHS

FOCAL NODULAR HIPERPLASIA
CT
Arterial , portal and hepatobiliary phase post GD-EOB-DTPA

FOCAL NODULAR HIPERPLASIA
DCE post GD-EOB-DTPA

ADENOMA : 25 Y/O FEMALE :GD-EOB-DTPA
Perfusion
Hepatobiliary phase

ADENOMA POST GADOLINIUM: 67 Y/O F

ADENOMA POST GD-EOB-DTPA: 67 Y/O F

OSLER –RENDU –WEBER POST GAD

METASTASIS BREAST GD-EOB-DTPA
Haemangioma

METASTASIS BREAST GD 6 MONTHS F/U

MULTIFOCAL FATTY DEPOSITION ,
HAMARTOMAS?

MULTIFOCAL FATTY DEPOSITION ,
HAMARTOMAS? GAD. AND GD-EOB-DTPA

LESIONS OF THE LIVER: CIRRHOTIC PATIENT
1. TYPICAL HEPATOCELLULAR CARCINOMA : “every hypervascular mass
in a liver with cirrhosis is HCC until proven otherwise “. T1W hypo / t2
slightly hyper; restricted diffusion ; DCE arterial enhancement ( 80%)
and wash-out . Large HCC- poorly differentiated-, may exhibit a broad
spectrum with mosaic pattern , capsule , “ nodule-in nodule “ or
extracapsular extension .
2. MACROREGENERATIVE NODULES: proliferating normal liver cells.
Poorly seen on CT ; Hyperintense on t1 ; no fat content so no signal
drop on out-phase ; almost never hyperinetnse on t2;free water
diffusion ; no enhancement or wash-out-wash-in
3. LOW GRADES DYSPLASTIC NODULES : still vascularised by the portal
vein , therefore isointense with the liver on arterial phase . Do not show
wash-out ; could be iso or slightly hyperintense using liver-specific
contrast . Could have tiny fatty component and drop in signal on out-
phase.

4.HIGH GRADE DYSPLASTIC NODULE: fatty changes with 10-20% signal
drop on out-phase ; slight degree of neo-angiogenesis ; hyperintense
on T2 ( macro-regenerative almost never) and t2 FS ; could be
hypointense in portal venous and late phase (wash-out).
5. HGDN versus HCC : NEOANGIOGENESIS AND FAT : T1
hypointense,
T2 hyperintense , signal decay on out-phase, restricted diffusion , early
arterial
enhancement and rapid wash-out . Hypointense on hepatobiliary phase .
6. WELL DIFFERENTIATED HCC : No restricted diffusion and enhances in
all phases including hepatobiliary of gadoxetate . Use subtraction
images if possible.
7. HCC may appear hyperintense on t1 due to haemorrhage; copper , fat or
glycogen.

CONFLUENT FIBROSIS : focal fibrosis sitting as a wedge-shaped lesion in
the anterior and medial segment of the liver ; geopgraphic patter, T1 low
, t2 high signal ; low signal on hepatobiliary phase .DD: infiltrative HCC
and cholangiocarcinoma .

LESIONS OF THE LIVER: CIRRHOTIC PATIENT :
HCC
1.Non -ring enhancing focus in the arterial
phase .
2.Occasional capsule
3.t2W hyperintense
4.Washout PRIMOVIST in the
hepatobiliary phase (washout is not
fade ).

MACRO REGENERATIVE NODULES GD-EOB-DTPA

MACRO REGENERAIVE NODULE 6 MONTHS
LATER GAD

MACRO REGENERATIVE NODULE 6 MOTH LATER
GAD

DYSPLASTIC NODULES GD-EOB-DTPA

MACROREGENERATIVE AND DISPLASTIC
NODULES DS-EOB-DTPA

CONFLUENT FIBROSIS BREAST CA POST CHEMO
30/04/18
01/07/18 12/03/19

LESIONS OF THE LIVER: AUTOIMMUNE
PANCREATITIS
- IgG4 sclerosing disease: mimic a cholangiocarcinoma with biliary
strictures and thickening involving any portion of the biliary tree, but
the common bile duct is the most affected . When the pancreas is
affected it shows a sausage like thickening with loss of lobulation and a
hypointense halo and rim enhancement .
- PRIMARY SCLEROSING CHOLANGITIS : idiopathic inflammatory
process with structure formation and distal bile duct dilatation and
beading appearances

LESIONS OF THE LIVER: CHOLANGIOCARCINOMA
Classification : Japan
1, Mass forming :signal depend of the proportion of fibrosis , necrosis and
mucin.
2, peri-ductal infiltration (Klastkin tumor)
3, intra-ductal ( distal CBD )
T1 hypo , t2 hyper intense , subtle peripheral enhancement , does not
enhance with the Gd-EOB-DTPA in hepatocellular phase due to lack of
hepatocytes but central extracellular uptake can be seen in the
dysplastic centre ( also in fibrous tissue of haemangioma and CRC
mets) .Associated findings: hepatic capsular retraction , dilatation of
peripheral bile ducts , satellite nodules, and vascular encasement
without grossly visible thombus
Reporting: longitudinal and radial spread, vascular involvement, lymph
nodes, mets , liver volume (Blumgart )

MAIN PANCREATIC DUCT LITHIASIS WITH TAIL
ATROPHY

MASS FORMING CHOLANGIO CA GD-EOB-DTPA

KLASTKIN TUMOR: PERIDUCTAL INFILTRATION

LEFT KLASTKIN TUMOR: GD-EOB-DTPA

FIBROTIC STENOSIS OR DYSFUNCTIONAL SPHINCTER
OF ODDI

GB TUMOR AS ACUTE CHOLECYSTITIS

PANCREAS : ANATOMY
THE GLAND :
1. Retroperitoneal but the tail extends into the peritoneum in front of the
spleen.
2. The pancreatic head is defined as being to the right of the SMV .
3. The pancreatic neck is located to the left of the head and ventral to the
SMV
4. The uncinated process is the prolongation of the medial and caudal part
of the head; it has triangular shape with a straight or concave
anteromedial border .
5. The overall characteristic are more important than the measurements:
lobular architecture , symmetry , signal intensity, enhancement , normal
duct and contour.

PANCREAS : ANATOMY
THE DUCTS:
1. The main pancreatic duct ap diameter: 3.5 mm head; 2.5 mm body ; 1.5 mm tail .
2. The main pancreatic duct (MPD) receives 20-30 side branches that enter the duct at right angles.
3. The downstream ductal configuration is the most common with a bifid end: Wirsung (ventral )
and Santorini (dorsal).
4. The duct of Santorini drains the anterior and superior portions of the head via the minor papilla.
5. MPD: 5 mm segmental or diffuse dilatation :
- 5 mm worrisome
- 10 mm , high risk stigma
In chronic pancreatitis : mm f/u
<10 mm 12 months
10-20mm 6-12 months
>20 mm 6 months

PANCREAS : ANATOMY
THE PANCREATOBILIARY UNION : Wirsung + CBD joints and drains in the
major papilla. Before entering the duodenum the are encircled by the
sphincter of Oddi, which measures 10-15mm in length which when
contracted could form a “pseudocalculus “ sign on MRCP . In most
cases the Wirsung + CBD form a short 5 mm channel with a distal
dilatation called the ampulla .

PANCREAS ENHANCEMENT
1. The pancreas demonstrates high T1 signal intensity and low T2 signal
intensity on pre-contrast images reflecting high protein content of the
exocrine gland. The pancreas demonstrates maximal enhancement on
hepatic arterial-dominant phase which fades on subsequent phases;
reﬂecting a normal capillary blush.
2. The pancreas shows a uniform capillary blush on the late arterial phase
images and fades on the subsequent hepatic venous and delayed
images. In patients with chronic pancreatitis, loss of aqueous protein in
the acini causes reduction of signal on fat-suppressed T1-weighted
images. The pancreas shows progressive enhancement that peaks on
the portal venous or interstitial phase. This finding is the result of
pancreatic fibrosis that causes impairment of capillary blood flow to the
gland.

PANCREAS ANATOMY : BRIGHT IN T1

ATROPHY OF THE VENTRAL PANCREAS

ATROPHY OF THE DORSAL PANCREAS

PANCREAS : BENIGN “NON-TOUCH “ ENTITIES
1. Pseudomasses due to fetal lobulations
2. Aberrant ductal configurations
3. Pancreatic cleft
4. Intrapancreatic accessory spleen.
5. Miscalls or Misdiagnosis : uneven pancreatic lipomatosis ,
determination of pancreatic cancer resectability ; accurate
measurement of cystic pancreatic lesions ; autoimmune pancreatitis
and inflammatory pseudotumors in chronic pancreatitic

MIMICS OF PANCREATIC CANCER
1. ANNULAR PANCREAS: pancreatic tissues encircles the second portion
of the duodenum; result from failure of normal pancreatic tissue to
rotated around the duodenum ; in children : gastro-duodenal
obstruction ; in adults : 50% asymptomatic .
2. LIPOMA OR FATTY INFILTRATION : lipoma has a capsule and contact the
peripancreatic fat .
3. INTRAPANCREATIC ACCESORY SPLEEN : follows the spleen signal in
all sequences

4. DUDENAL HAEMATOMA
5. PARA-DUODENAL PANCREATITIS OR GROOVE PANCREATITIS : (CYSTIC
DYSTROPHY OF DUODENAL WALL ) :pancreatitis in and around the
duodenal wall near the minor papilla (para-duodenal wall cyst) . In young
alcoholic males with abdominal pain , weight loss, nausea and vomiting :
solid fibrotic mass around the minor papilla or a cyst in the duodenum .
Duodenal stenosis , biliary structures, chronic calcifying pancreatitis and
pancreatic duct dilatation .
Mass forming : difficult to differentiate from pancreatic cancer : even the
biopsy could be misleading if you biopsy the fibrous tissue : thickened
duodenal wall.
Both , mass forming pancreatitis and pancreatic ca show delayed
enhancement on CT and MRI due to fibrosis ; a well defined mass favours ca
; imaging features of non-dilated and smooth tapering pancreatic and bile
ducts coursing though the mass ( duct penetrating sign “), pancreatic duct
irregularity , and the presence of calcifications favour chronic pancreatitis

5. PANCREATIC CARCINOMA ON A BACKGROUND OF CHRONIC
PANCREATITIS
6. AUTOIMMUNE PANCREATITIS : periductal infiltration with IgG4-
posistive plasma cells (In type II ): narrowing of the pancreatic duct and
acinar atrophy : diffuse , focal and multifocal. In diffuse, sausage
shaped with loss of the lobular contour, smooth contour and
hypointense halo sign.
7. Progressive pancreatic duct dilatation .

FOCAL FATTY REPLACEMENT HEAD PANCREAS

SPLENUNCULUS IN THE TAIL OF PANCREAS

DUODENAL HAEMATOMA MIMIKING
PANCREATIC CANCER

PERIAMPULAR DIVERTICULUM : CBD
DILATATION

PARADUODENAL PANCREATITIS OR CYSTIC
DYSTOPHY OF THE DUODENAL WALL

AUTOIMMUNE PANCREATITIS
Loss of fatty cleft and reduced enhancement

PANCREATITIS AND FAT SAPONIFICATION

PROGRESSIVE PANCREATIC DUCT DILATATION
:DUCTAL EPITHELIAL HYPERPLASIA
/DYSPLASIA

CYSTIC PANCREATIC LESIONS
THE PREOPERATIVE DIGNAOSIS IS DIFFICULT .
DIFFERENTIAL DIAGNOSIS :
A. NON NEOPLASTIC PANCREATIC CYST :
1. PSEUDOCYST: is the most common 80-90% ; amylase –rich fluid ;
fibrous wall without epithelial lining, after 4-6 post acute attack ; smooth
/thin/thick wall with uniform thickness ; complications : infection,
haemorrhage, rupture and obstruction of other organs
2. Lymphoepithelial cyst
3. Epidermoid cyst
4. Mucinous nonneoplastic cyst of the pancreas (MNNC): uni or
lobulated , thin-walled with thin septa , no calcification , no mural
nodules or communication with MPD . Can grow but no malignant
potential . C19-9, CEA and amylase are normal.

B. NEOPLASTIC CYSTIC LESIONS
1. SEROUS CYSTADENOMA :women over 60 years ; in the pancreatic
head, lobulated contour, lack of wall enhancement , Could show
honeycombing appearance, septa and internal calcification and scar
.On US and CT looks solid; on MRI slightly hypervascular (stroma); a
variant called macrocystic is very difficult to differentiate from
mucinous cystadenoma .
2. MUCINOUS CYSTIC NEOPLASM :almost exclusively of women; fifth
decade ; body tail of the pancreas ; the most common cystic tumor of
the pancreas ;made of large cystic spaces lined by tall mucin-producing
columnar cells ; uni or multilocular . On US smooth external surface
with cystic appearance; CT/MRI: multiple enhancing septations and
solid intramural nodules; solid papillary excrescences protruding from
the wall . T1 low signal ; t2 haste high ; DWI/ADC high .

3. INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM: both sex over 60 years ,
exocrine mucin-producing tumours with cystic dilatation of a main or a side
branch duct that contains thick mucoid secretion .
3.1 .IPMN main duct type: MRCP demonstrate communication with the main
duct with clubbed (like a black trefoil leaf on playing cards) and finger -like
appearance of the cyst. High risk .
3.2. IPMN branches type: MRCP: uncinated process, grapelike appearance
and communicating with the duct . If the cystic component is bright on FS
think on haemorrhage . Less risk.

3. INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM
3.3. IPMN mixed type. High risk
Comment: If > 3 cm, papillary projection or the duct >10 mm : excision
4. SOLID AND PAPILLARY EPITHELIAL NEOPLASM : or papillary and cystic
tumour; mainly in young black or Asiatic woman .

PSEUDOCYST OBSTRUCTING THE CBD

CYST IN THE BODY :?MUCINOUS , PSEUDO-
PAPILLARY , LYMPHO-EPITHELIAL

MULTIPLES CYSTS : CHRONIC PANCREATITIS

PANCREATIC CARCINOMA : MRI
1. The normal pancreas must be brighter than the liver on t1.
2. SIGNAL INTENSITY ON MRI: DCE
t1fs ARTERIAL VENOUS
LATE
NORMAL PANCREAS bright bright low low
CANCER low low brighter
brighter
The delayed enhancement is secondary to fibrosis

PANCREATIC CARCINOMA
1. TUMOR SIZE: organ confined T1 , 2cm; T2 > 2 cm; potentially
resectable.
2. LOCATION : to the RIGHT of the SUPERIOR MESENTERIC VEIN ,
pancreatic head and uncinated process ; to the LEFT of the origin of
the SMV: pancreatic body al tail for distal pancreatectomy .
3. EXTENSION BEYOND THE PANCREAS: is there a vascular contact?
EXOPHYTIC TUMORS: T3
SUPERIOR MESENTERIC VEIN: circumferential contact (<180 0r >= 180
degrees); irregular vessel contour , focal narrowing , extension into the
vessel lumen, thrombus .
TEAR DROP SIGN : invasion of the adventitia with length of contact in
coronal and sagittal . T3 , but borderline resectable : the fat line
between the splenic or portosplenic confluence or portal vein is effaced.

PANCREATIC CARCINOMA
3. EXTENSION BEYOND THE PANCREAS :
Arterial contact: coeliac axis, common hepatic artery, SMA(<180; >= 180). If
the gastroduodenal artery is encased it does not preclude surgery, hence
borderline resectable . It would be resected in block in the Whipple
procedure.
Encasement of all other arteries : T4: unresectable.
4. ADJACENT ORGANS INVASION: IVC, aorta, adrenals , kidney, spleen,
stomach, colon , mesocolon or small bowel .
5.METASTASIS : lymph nodes , local or distant ; liver , peritoneal space (
mesentery , omentum , ascites , “sister Joseph” nodule withing the
umbilicus , lungs .
The nodal staging remains a challenge for MDCT ; all peripancreatic nodes are
removed in block.
For peritoneal staging , laparoscopy is the procedure of choice .

NO VISIBLE TUMOR BUT DILATATION OF MPD
.0
Ct KUB
3 months

3 months

Mild pancreatitis
One months
Truncated MPD

PET-CT

EARLY PANCREATIC CA
Whipple procedure

BORDERLINE PANCREATIC TUMOR
1 year

NEUROENDOCRINE TUMORS
1. INSULINOMA : 90% < 2 cm ; 90% benign ; 90% single. The most
common but only 3 cases /million ; most often hypervascular . Not all
are visible on DCE so use T1W 2D GRE (FLASH, FFE ) with FS .
Sometimes Whipple triad: fasting hypoglycemia, symptoms of
hypoglycemia ,relief after IV glucose.
2. GASTRINOMA :in the gastrinoma triangle: are between the junction of
the cystic and common hepatic duct superiorly; the inferior duodenal
flexure inferiorly and the pancreatic neck medially . Some times
Zollinger-Elliosn ulcer, massive gastric fold thickening , elevated serum
gastrin and hyperclorhydria .50-80% are well differentiated carcinomas ;
benign < 1 cm , malignant > I 1cm with increase expression of
somatostatin receptor (SSTR).
3. VIPOMA; always malignant ; severe diarrhoea ; big tumor with jaundice;
biliary duct dilatation is not common .
4. Glucagonoma and Somatostatinoma

NEUROENDOCRINE TUMORS
Hydro-CT : 1.5 L water; some tumour would be in the duodenal wall; arterial
phase
Aortic transit 15 sec.
PREDICTIVE NON BENIGN : > 3 cm ; calcification , vascular invasion , solid
cystic appearances ; heterogeneous low enhancement .

NEUROENDOCRINE TUMOR AMPULLA
Octreotide scan

MIXED DUCTAL NEUROENDOCRINE CARCINOMA

TAKE HOME POINTS
1. Standard sequences in the liver + DWI + DCE with gadolinium is
superior that CT in characterisation of the liver lesions .
2. DCE with Gd-EOB-DTPA , hepatic-specific agent , could help
differentiating between FNH , adenoma , haemangioma and HCC .
3. In a cirrhotic liver , finding a fast enhancing lesions with wash out
suggest HCC until proven otherwise .
4. The transition from hyperplastic nodule to dysplastic nodule to HCC is
forged incorporating fat and neo vascularity .
5. A dilated main pancreatic duct could be the unique sign of an early
pancreatic cancer.

REFERENCES
International Cancer Imaging Society ; Interactive: Masterclass in Imaging of Hepatobiliary Tumours .Friday
8th April 2016
International Cancer Imaging Society; Interactive: Masterclass in Imaging of Pancreatic Tumours: 3rd
November 2016.
Abdominal Radiology . Vol42.Number 12 , December 2017
Behroze Vachha et al. Cystic Lesions of the Liver .AJR.2011;196:W355-W366
Bayer HealthCare :Liver-specific hepatobiliary contrast agent for MRI of focal liver lesions ; December 2011.
Jose Traila Campos, Claude b. Sirlin . Jin-Young Choi. Focal hepatic lesions in Gd-EOB-DTPA enhanced MRI:
the atlas . Insights Imaging (2012)3:451-474
Paul Nikolaidis et al. Imaging Features of Benign and Malignant Ampullary and Periampullary Lesions
.RadioGraphics 2014; 34:624-641
Mahmoud M . Al-Hawary, Isaac R.Francis. Pancreatic ductal adenocarcinoma staging.Cancer Imaging (2013):
13 (A), 57-61
Young H. Kim et al. Imaging Diagnosis of Cystic Pancreatic Lesions: Pseudocyst versus Nonpseudocyst.
RadioGraphics 2005; 25: 671-685
Mary Ann Turner, Ann S. Fulcher. The Cystic Duct :Normal Anatomy and Disease Processes. RadioGraphics
2001; 21 : 3-22
Koenraad J. Mortele. Mimics, Miscalls, and Misses in Pancreatic Disease. The Radiology M and M Meeting :
Misinterpretations , Misses , and Mimics. Harvard .

Quick review of hepatobiliary and pancreatic lesion

Quick review of hepatobiliary and pancreatic lesion

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