CT and MRI findings in chronic pancreatitis: what should the

radiologist know

Poster No.: C-1392

Congress: ECR 2013
Type: Educational Exhibit
Authors: I. G. Lupescu, G. Popa; Bucharest/RO
Keywords: Abdomen, Pancreas, CT, MR, Education, eLearning, Inflammation,
Education and training
DOI: 10.1594/ecr2013/C-1392

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Learning objectives

• To present and illustrate the typical (Fig. 1 on page 3) and particular CT

and MRI aspects encountered in chronic pancreatitis (CP).

• To list and describe the main complications of CP (Fig. 2 on page 3).

• To discuss and illustrate the differential diagnosis of CP (Fig. 3 on page

4).

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Images for this section:

Fig. 1: Chronic pancreatitis- typical CT (a) and MRI (b) findings: main pancreatic duct
dilatation; Wirsung duct lithiasis (arrows); pancreatic calcifications; pseudocysts (Ps).

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 2: Complicated chronic pancreatitis. Enhanced CT evaluation (a-d): atrophy of
the pancreatic tissue, calcifications, huge pseudocyst of the pancreatic cephalic region
(arrow) with compression of the choledoc and biliary tree obstruction- note intrahepatic
biliary ducts dilatation(arrowhead); portal cavernoma (black arrow).

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 3: Cephalic pancreatic adenocarcinoma: MRI evaluation T1wi(a,b), MRCP(c):
small hypointens T1 nodule of the pancreatic head (arrow) with positive double duct
sign (obstruction and dilatation of the main pancreatic duct and of the choledoc-
arrowhead);body and tail pancreatic atrophy

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Background

DEFINITION. Chronic pancreatitis (CP) represents a continuing inflammatory disease

of the pancreas characterized by irreversible morphologic and functional (exocrine and
endocrine) changes (1-3).

INCIDENCE. The incidence of CP is about 27:100.000, with a considerable geographic

variation (3).

CAUSES

• Alcohol abuse is the main cause of CP (70-80% of cases)

• Others causes: smoking hyperlipidemia, hyperparathyroidism, trauma.
• About 20-30% of cases have no clear etiology and are classified as
idiopathic (1-3).

TYPES of CP

• Chronic calcifying pancreatitis- most common

• Chronic obstructive pancreatitis (pseudotumoral CP)
• Autoimmune pancreatitis
• Groove pancreatitis
• Metabolic forms of CP
• Hereditary forms of CP
• Tropical pancreatitis
• Idiopathic chronic pancreatitis (4)

Chronic calcifying pancreatitis (CCP) is related to alcoholism (5). The earliest finding
is precipitation of proteinaceous material in the pancreatic ducts that forms protein
plugs that subsequently calcify (3). The ducts and lobules are initially involved in
a random manner. Many of the small pancreatic ductules dilate, while others are
obliterated by fibrosis. The main pancreatic duct has a chain-of-lakes appearance due
to alternating stenoses and dilatation. In approximately 50% of patients with chronic
calcifying pancreatitis, the pancreatic parenchyma contains cysts of varying sizes
(several millimeters to 5 cm). These cysts are lined by cuboidal epithelium and contain
pancreatic enzymes. Peripancreatic fibrosis generally is a late finding that involves the
portal and/or splenic veins. Ascites may complicate CCP as a result of portal hypertension
or lymphatic obstruction in 1-2% patients (3,4).

Chronic obstructive pancreatitis (COP), consists in periductal fibrosis and subsequent

ductal dilatation. In most patients, the changes involve only the portion of the pancreas
in which ductal drainage is impaired. Diffuse changes may occur, in which the main
pancreatic duct or ampulla is obstructed (6,7). Calcification is unusual. Moreover, the

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pancreatic duct is dilated, and the pancreas is normal in size, atrophic, or focally and/
or globally enlarged. A variety of factors are implicated in COP; these include ductal
obstruction due to ampullary stenosis, inflammatory or neoplastic causes, surgical ductal
ligation, and fibrosis (2-4, 6).
Autoimmune Pancreatitis known also as lymphoplasmacytic sclerosing pancreatitis,
chronic sclerosing pancreatitis, pseudotumorous pancreatitis, or nonalcoholic duct-
destructive CP is a type of chronic pancreatitis that is characterized by an autoimmune
inflammatory process, with lymphoplasmacytic infiltration associated with fibrosis of
the pancreas (8,9). Clinical features include: jaundice (63% of cases), abdominal pain
(35%), weight loss (35%), and diabetes mellitus (42%-76%). This entity include absence
of classic acute attacks of pancreatitis, elevated immune markers (immunoglobulin
G4) and dramatic response to steroid therapy/ Autoimmune pancreatitis represent a
difficult diagnostic particular in differentiating it from pancreatic cancer. Others associated
pathologies include: biliary diseases such as sclerosing cholangitis and primary
biliary cirrhosis (68%-88% of cases); inflammatory bowel disease (most commonly,
ulcerative colitis) (17%); Sjögren syndrome; sialadenitis (12%-16%); renal involvement
(3.4%-35%); and retroperitoneal fibrosis (3%-8%). Typical CT characteristics include:
diffuse or focally enlarged pancreas with 'halo' of low density, 'sausage' like gland, loss of
fatty lobulation, minimal pancreatic stranding and stricture of common bile duct +/- intra-
hepatic ducts (8,9).

Groove Pancreatitis (GP) is a rare form of chronic pancreatitis that may mimic
pancreatic adenocarcinoma. The term pancreatico-duodenal groove refers to the
potential space between the head of the pancreas, the duodenum, and the common
biliary duct (CBD). There are two forms of GP: the "segmental" form, which involves the
pancreatic head with development of scar tissue within the groove; and the "pure" form,
which affects the groove only, sparing the pancreatic head. Clinical manifestations are
related to duodenal and biliary obstruction. Several factors such as peptic ulcer disease,
gastric resection, true duodenal wall cysts, pancreatic heterotopia, and disturbance of
flow in the main pancreatic duct are related to the development of GP (10-12).
"Paraduodenal pancreatitis" has been proposed to include groove pancreatitis, cystic
dystrophy of the duodenal wall, and paraduodenal wall cysts. All of these entities occur
in and around the minor papilla and may mimic the pancreatic cancer in terms of clinical
and imaging appearance (13).

Tropical Pancreatitis is a variant of CP with a regional predisposition in tropical countries

that appear in young people associated with malnutrition, rapid progressive course with
severe pancreatitis, the presence of large intraductal calculi, and an increased risk of
adenocarcinoma (4).

Hereditary pancreatitis is an autosomal dominant disease involving mutation of the

cationic trypsinogen gene and accounts for less than 1% of cases of recurrent and CP.
As in tropical pancreatitis, acute attacks begin in childhood (5-10 years of age), with age
th
at onset varying from infancy to the 5th or 6 decade of life. These recurrent attacks

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result in CP with parenchymal and ductal calcifications, duct destruction, and secondary
exocrine and endocrine pancreatic insufficiency (3,4,14).

Idiopathic chronic pancreatitis (ICP) occur in patients without an apparent cause.

Early-onset ICP has a different natural history from late-onset ICP; early-onset ICP is
characterized by severe abdominal pain during the first 2 decades of life (2-4).

PHYSIOPATHOLOGY (main mechanism): intraductal precipitation of calcified

concretions with obstruction and scar formation (3).

SYMPTOMS

• epigastric pain,
• weight loss,
• signs of malabsorbtion,
• steathoreea (80%),
• diabetes (58%). (3)

RADIO-IMAGING METHODS:

Ultrasound

• Inhomogeneity of the pancreatic parenchyma: initial stage

• Atrophy of the pancreatic parenchyma
• Pancreatic main duct dilatation; concretions (3)

Computed Tomography (CT)

• Diffuse or circumscribed enlargement of the pancreas: early phase and in

acute inflammation
• Atrophic parenchyma: later phase
• Dilatation of the intrapancreatic ducts (Fig. 4 on page 12)
• Calcifications:+++
• Pseudocysts; cysts (3,15)

Magnetic resonance imaging (MRI) and MR chlangiopancreatography (MRCP)

• Decrease signal T1 intensity of the pancreatic tissue

• Decrease of the contrast enhancement of the pancreatic tissue due to
fibrosis
• Main pancreatic duct (MPD) and side branches changes: better seen on
T2wi (Fig. 5 on page 12) and MRCP (Fig. 6 on page 13)
• Intraductal concretions
• Pseudocysts;cysts (3,4)

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Despite a good image quality, MRCP may result in a high number of false-negative
findings in the assessment of the pancreatic ducts because of the small size of the main
pancreatic duct (especially in the tail of the pancreas) and of the side branches (16-18).
Exogenous administration of secretin stimulates the exocrine pancreas in the production
of fluid and bicarbonates that accumulate inside the pancreatic ducts and thus improves
visualization of the pancreatic duct at MR cholangiopancreatography (19).

Diffusion-weighted MRI in CP using high b-value has evolved as an additional imaging

modality, which measure changes in the tissue water diffusion. Compared to the normal
pancreatic parenchyma, ADC in CP is lower, wich may be explaind by fibrosis, chronic
inflammation and reduction of pancreatic exocrine tissue (23).

ERCP

Provides the most precise images of ductal changes (Fig. 7 on page 14)

• changes in the main pancreatic duct

• changes in the side branches
• intraductal concretions (7)

Cambridge classification (Axon, 1989)

• mild CP- at least three abnormal side branches

• moderate CP-changes of the main pancreatic duct ( Fig. 8 on page 15 )
• marked CP- addition of one or more of the following signs: severe dilatation
of the pancreatic duct (more than 1 cm); obstruction; marked mural
irregularity; intraductal filling defects; opacification of large cavity (>1 cm).

ERCP is important in intervention procedures (3)

Endosonography

Precise visualization of the parenchymal and ductal changes (3)

Plain abdominal radiography

• Non longer use in the diagnosis of CP (3).

• May show calcifications projected into the pancreatic area ( Fig. 9 on page
16 ).

PATHOGNOMONIC IMAGING SIGNS:

• Atrophy of the pancreatic parenchyma

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 • Changes of the main pancreatic duct, changes in side branches, intraductal
concretions

BEST IMAGING MODALITIES:

• MRI with MRCP

• CT especially in complicated CP

COMPLICATIONS:

• Pseudocysts
• Vascular: pseudoaneurysm, venous thrombosis
• Fistula
• Biliary obstruction in focal inflammatory pancreatic mass

Pseudocysts (PS) are encapsulated (by fibrous tissue) fluid collection located in the
pancretic area or migrated away from the pancreatic tissue.

Incidence. PS represents 90% of all cystic pancreatic masses and 10%-15% in chronic
pancreatitis.
Location: Most commonly pseudocysts are located in the anterior pararenal space and
omental bursa.

Complications: rupture and fistula formation into the abdominal cavity, stomach;
hemorrhage (with or without pseudoaneurysm); infection (2,3).

Vascular complications

Arterial complications: pseudoaneurysm produced by pancreatic or peripancreatic

blood vessel erosion (autodigestion of arterial walls by enzymes liberated in pancreatitis).
Pseudoaneurysm may develop within a preexisting pseudocyst. The most affected
arteries are the splenic and the gastroduodenal (2,3).

Venous Thrombosis characterized by absence of flow void, no enhancement at CT and

MR venography, presence of venous collaterals (3).

Fistula. Pancreatic fluid may penetrate organs and cavities and create fistulas: pleura
via the lesser sac and the aortic or esophageal hiatus; peritoneum via the lesser sac and
foramen of Winslow leading to a pancreatic ascites.

DIFFERENTIAL DIAGNOSIS:

• pancreatic adenocarcinoma- the two diseases may coexist.

• intraductal papillary mucinous tumors
• acute pancreatitis (3,21,22)

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COURSE and PROGNOSIS. In chronic pancreatitis exocrine and endocrine insufficiency
appear. Increase the incidence of pancreatic adenocarcinoma.

PITFALLS. CP may be misinterpreted as a pancreatic adenocarcinoma (3,7).

Pseudotumoral CP versus pancreatic carcinoma, remains a difficult diagnosis.

Decreased T1 signal intensity with delayed enhancement after gadolinium administration
in association with dilatation and obstruction of the pancreatico-biliary ducts can be
seen in both diseases (3). Irregularity of the pancreatic duct, intraductal or parenchymal
calcifications, diffuse pancreatic involvement, and normal or smoothly stenotic pancreatic
duct penetrating through the mass ("duct penetrating sign") favor the diagnosis of chronic
pancreatitis over cancer (6,21,22). In distinction, a smoothly dilated pancreatic duct with
an abrupt interruption, dilatation of both biliary and pancreatic ducts ("double-duct sign"),
and obliteration of the perivascular fat planes favor the diagnosis of cancer (2,22).

THERAPEUTIC OPTIONS

• Surgery is indicated in complicated CP and severe abdominal pain;

• Endoscopic procedures: removal of pancreatic duct stones; stenting for
stenosis of the bile duct or for severe strictures involving the main pancreatic
duct (3).

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Images for this section:

Fig. 4: Calcified chronic pancreatitis. Enhanced CT evaluation in axial plane(a,b) and

coronal plane(c,d): atrophy of the pancreatic tissue, multiple pancreatic calcifications,
dilatation and moniliform aspect of the main pancreatic duct (arrow).

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 5: Chronic pancreatitis: MRI evaluation in T2wi(a,b) and T1 after Gd-BOPTA (c,d)
contrast injection: pancreatic main duct dilatation (arrow); reduction of the pancreatic
tissue enhancement; hypertrophy of the pancreatic head.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 6: Chronic pancreatitis: MRCP evaluation- important changes of the main pancreatic
duct (arrow) and of its side branches: important and irregular dilatation of the main
pancreatic duct, cystic dilatation of the side branches of the pancreatic duct

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 7: Chronic pancreatitis: ERCP evaluation: double duct sign positive (dilatation of the
CBD-arrow and of the MPD-arrowhead); small filling defects in the main pancreatic duct.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 8: Abnormalities of the main pancreatic duct in chronic pancreatitis: normal (a); mild-
small irregularity (b); pronounced irregularities of the pancreatic duct contur (c); "chain
of lakes" (d).

© Scheme modified after Van Hoe L et al. Atlas of cross sectional and projective MR
cholangiography, Springer 2001, 337

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Fig. 9: Plain abdominal radiography centered on the epigastric-mesogastric area:
multiple small nodular calcifications projected into the pancreatic zone.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Imaging findings OR Procedure details

MATERIAL and METHODS

Retrospective study on 115 patients (85 male patients, 30 females patients (Table 1
on page 23) aged between 9 and 75 years (mean age 55 years old) diagnosed with
CP in the last 10 years, explored by CT (68% of cases) and by MRI including MRCP
acquisitions (32% of cases). In 22 % of cases explored by CT, we have performed in
addition an MRI evaluation to better characterise the changes that have involved the
pancreatic region.

Causes. In about 65% of cases there was a context of alcohol abuse. Hyperlipidemia
was present in 11% of patients with CP. Hyperparathyroidism was associated in 1,5% of
patients with CP. Autoimmune pancreatitis was found in 1,7% cases. About 21% of cases
did not have a clear etiology and were classified as idiopathic (Table 2 on page 23).

TECHNIQUES

Multislice CT. Unenhanced MSCT series were programmed to include the upper
abdomen. The upper and lower MDCT scanning levels were chosen using these
unenhanced CT images. All patients underwent unenhanced MDCT followed by arterial
phase, pancreatic parenchymal phase, and PVP imaging. All patients received 1,5 mL/
Kg of a nonionic iodinated contrast (350 I mg/mL,) with a monophasic injection using a
power injector. The contrast material was administrated at a rate of 3 mL/s in all patients.
Phase acquisition was initiated 25 seconds for the arterial phase, 40 seconds for the
pancreatic parenchymal phase, and 70 seconds for the portal venous phase after the
injection of contrast material began.

MRI. To evaluate the pancreatic parenchyma and the pancreaticobiliary ductal system,
we have used T1-weighted FSPGR FS and T2-weighted FSE FS in axial plane; T2 ssFSE
short TE in coronal and oblique plane; 2D MRCP; and T1-weighted 3D FAME before and
after gadolinium (0.1 ml/kgc) in arterial, pancreatic phase and venous phase.

IMAGING SIGNS

CT findings (Table 3 on page 24)

• Calcifications were found in 63 % of CP cases. Intrapancreatic calcifications

were focal (in 51% of cases) or diffuse (12%), punctate or (micro)nodular.

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 CT has the higher accuracy for detecting calcifications which are a specific
sign of severe and advanced CP.
• Wirsung duct anomalies (dilatation, contour irregularities and moniliform
aspect) were visualized in 68% of cases.
• Pancreatic diffuse atrophy was detected in 43% of cases
• Focal hypertrophy of the pancreas was found in 17% of cases.
• Pseudocysts were detected in 22% of cases.
• Decrease enhancement of the pancreatic tissue was observed in 81% of CP
cases.

MRI findings (Table 4 on page 24)

• Wirsung duct anomalies (dilatation, irregularities of the contour and

moniliform aspect) were visualized in 87% of CP cases.
• Wirsung duct concretions were visualized in 21,5% of cases.
• Pancreatic diffuse atrophy was detected in 31,5% of cases.
• Focal hypertrophy of the pancreas was found in 16% of cases.
• Pseudocysts were detected in 7% of cases.
• Decrease enhancement of the pancreatic tissue was observed in 79 % of
cases.

CT and MRI common findings

• Enlargement of the pancreatic tissue (early stage)-Fig. 10 on page 25

• Atrophy of the pancreatic tissue (late stage)- Fig. 11 on page 26, Fig. 12
on page 27
• Strictures and dilatation of the MPD- Fig. 13 on page 28, Fig. 14 on page
29
• Intrapancreatic calcifications: best seen by CT-Fig. 15 on page 30, Fig.
16 on page 31
• Main pancreatic duct concretions: best seen by MRCP- Fig. 17 on page
32
• Pseudocysts- Fig. 18 on page 33
• Inflammatory pseudotumor (focal pancreatic hypertrophy)- Fig. 19 on page
34

Comparison between CT and MRI findings in CP evaluation

• Main pancreatic duct abnormalities (alternation of strictures and dilatations):

MRCP > CT
• Main pancreatic duct lithiasis: MRCP> CT
• Parenchymal pancreatic calcificatins: CT > MRCP
• Pseudocyst: MRCP = CT
• Communication between pseudocyst and the main pancreatic duct: MRCP >
CT
• Inflammatory pseudotumor versus pancreatic carcinoma: MRCP ≥ CT

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CHRONIC PANCREATITIS FORMS

• Calcifying chronic pancreatitis (diffuse calcifications: 12 % of cases)

• Obstructive CP with inflammatory mass was present in 16,8% of cases.
• Groove pancreatitis and cystic dystrophy of the duodenum was retrieve in
0,5% of cases.
• Autoimmune pancreatitis mimicking a tumoral process of the pancreas was
found in 2 cases

Calcifying chronic pancreatitis (CCP): calcifications, cysts, Wirsung duct dilatation with
a a chain-of-lakes appearance (Fig. 20 on page 35 ).

Obstructive CP with inflammatory mass: most commonly the inflammatory mass was
located in the pancreatic head.

• CT: calcifications within the mass (Fig. 21 on page 36)

• MRI features (Fig. 22 on page 37) : positive double duct sign-dilation
of the main pancreatic duct distal to the site of stenosis associated with
obstruction and dilatation of the choledoc and biliary tree;
• Abnormal side branches distal to the site of stenosis
• Intraductal stones
• Pseudocysts at different locations
• Side branches: nipping, clubbing, distorted appearance
• Duct-penetrating sign dilated side branches traversing the suspect area
• Hyperintensity focal mass on non-fat-suppressed T1w images
• Focal mass not presenting as a "black hole" on early-phase dynamic
contrast-enhanced images.

Groove pancreatitis and cystic dystrophy of the duodenum. All of the 6 cases
showed duodenal-wall thickening, associated with cysts in the groove or/and duodenal
wall. The cysts ranged from 5 mm to 4 cm. Cysts were well demonstrated on T2-
weighted, postgadolinium T1 FS wi and MRCP images. CT with contrast injection and fat
suppressed T1 w images revealed the best delineation of the pancreatic head from the
hypointense mass in the pancreaticoduodenal groov (Fig. 23 on page 38).

Autoimmune pancreatitis. MR imaging revealed diffuse enlargement of the gland with a

peripheral high signal rim on T2 wi and homogeneous T1 enhancement. MRCP showed
a diffuse narrowing of the pancreatic duct, and strictures of the pancreaticobiliary tree.
Narrowing of the superior mesenteric vein, splenic vein, main portal vein was seen
in both cases (Fig. 24 on page 39). Follow-up using MR imaging demonstrates
significant reduction of the "pancreatic inflammatory pseudotumor" after 4-6 weeks of
steroid therapy (Fig. 25 on page 40). 1 case developped after 3 years retroperitoneal
fibrosis (Fig. 26 on page 41).

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COMPLICATIONS. 44,73 % of CP cases presented complications. In descending order
complications of CP were represented by:

• pancreatic pseudocysts,
• biliary obstruction,
• venous thrombosis
• pseudoaneurysm
• fistula (pancreatic ascites)

Pancreatic pseudocysts were found in 19,5% of CP cases. In 98% of pancreatic

pseudocysts, the content presented the same intensity as

water (Fig. 27 on page 42, Fig. 28 on page 43), and in 2% the content had variable
attenuation coefficient/mixed signal intensity if hemorrhagic, blood clot, cellular debris
(Fig. 29 on page 44).

Biliary obstruction was present in 17,5% of CP cases secondary to a inflammatory mass

located into the pancreatic head (Fig. 30 on page 45) or a compressive pancreatic
pseudocyst.

Venous thrombosis was found in 3,4% of CP cases, involving the superior mesenteric
vein territory (Fig. 31 on page 46), the splenic vein or the portal vein.

Pseudoaneurysm was visualized in 2,6% of CP cases (Fig. 32 on page 47).

Pancreatic ascites was present in 1,73% of CP cases (see Fig. 28 on page 43 and
Fig. 29 on page 44).

DIFFERENTIAL DIAGNOSIS. Differential diagnosis must be done:

• in pseudotumoral forms of CP with pancreatic carcinoma,

• in cases with important dilatation of Wirsung duct and side branches with
intraductal papillary mucinous neoplasm and
• in diffuse pseudotumoral forms with acute pancreatitis.

Pancreatic adenocarcinoma. Most adenocarcinoma originate in the main pancreatic

duct and cause ductal obstructionthat occurs early and associate variable degree of
parenchymal atrophy and small intrapancreatic pseudocysts in 10% of cases ( Fig. 33
on page 48 ).

Intraductal papillary mucinous neoplasms.Typical appearance of the main duct type

is characterised by marked global dilation of the main pancreatic duct (greater than 15
mm) without a demonstrable cause of obstruction. Branch duct type is represented by
a "Polycystic" mass in the uncinate process, actually representing focally dilated side
branches filled with mucin ( Fig. 34 on page 49 ).

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Acute pancreatitis. Extensive peripancreatic fluid collection without pancreatic
parenchymal atrophy ( Fig. 35 on page 50 ).

WHAT THE RADIOLOGIST MUST REPORT

• the shape, dimensions and structure of the pancreas (Fig. 36 on page

50)
• the degree of the pancreatic tissue enhancement
• the presence of calcifications
• the presence of pancreatic cysts/pseudocysts (Fig. 37 on page 51)
• the existence of main pancreatic duct dilatation (moniliform aspect) +/-
dilatation of biliary tree (see Fig. 37 on page 51)
• the presence of a focal hypertrophy (inflammatory mass)
• adjacent vascular structures analysis (thrombosis,portal hypertension)
• complications: acute inflammation signs (necrosis, fluid collections,
pseudocysts); vascular thrombosis;pseudoaneurysm (Fig. 38 on page
52) ; fistula
• particular forms of CP (Fig. 39 on page 53)
• others incidental abnormalities (Fig. 40 on page 54)

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Images for this section:

Table 1: Distribution of chronic pancreatitis in Fundeni Clinical Institute- Male/Female

ratio: 2,8/1

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Table 2: Causes of chronic pancreatitis in Fundeni Clinical Institute

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

Table 3: Chronic pancreatitis: CT findings

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Table 4: Chronic pancreatitis: MRI findings

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 10: Early stage of chronic pancreatitis: global enlargement of the pancreatic tissue
in T1 and T2 w images (arrow). Note the decrease of signal intensity in T1 FSPGR FS
sequence.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 11: Late stage of chronic pancreatitis- CT evaluation: important atrophy of the
pancreas, Wirsung duct dilatation (arrowhead), pancreatic nodular calcifications (arrow).

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 12: Late stage of chronic pancreatitis-MRI evaluation (T1 FS, T2 and MRCP):
important atrophy of the pancreas (arrow), dilatation and irregularity of the main
pancreatic duct (arrowhead), dilatation of the side branches.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 13: Chronic pancreatitis- enhanced CT evaluation: enlargement and irregularity of
the main pancreatic duct (arrow); decrease enhancement of the pancreatic parenchyma;
ascites; left renal subcapsular fluid collection (arrow head).

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 14: Main pancreatic duct abnormalities- ssFSE short TE (a,b,c) and long TE (d):
alternation of important dilatations and stenoses involving the Wirsung duct (arrow head)
associated with small lacunar images that correspond to intraductal calcification(long
arrow)and intrapancreatic cysts.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 15: Multiple pancreatic calcifications (arrowhead), Wirsung duct dilatation,
hypertrophy of the pancreatic head with moderate biliary obstruction(dilatation of the
choledoc and of the gallbladder)- enhanced CT evaluation

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 16: Chronic pancreatitis- typical enhanced CT and MRI (T1, MRCP) findings:
Wirsung duct dilatation (long arrow) and side branches, pancreatic calcifications (seen
at CT), cysts of the pancreatic head (arrowhead) with discrete biliary obstruction
(compression of the CBD).

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 17: Intraductal concretions visualized using MRCP (ss FSE long TE) and short TE:
dilatation, irregularities of the main pancreatic duct associated with multiple hypointense
intraductual lacunar images (long arrows)

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 18: Pancreatic pseudocyst with mass effect on the stomach- MRI evaluation (T2 wi
FS, MRCP): retrogastric encapsulated fluid collection (long arrow); note small cysts into
the head of the pancreas

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 19: Pseudotumoral form of chronic pancreatitis: hypertrophy of the pancreatic head
(long arrow) associated with positive double duct sign: contrast enhanced CT evaluation
(the top part of the image) and MRI evaluation (the bottom part of the of the image in T2
wi and MRCP); small lacunar images in the main pancreatic duct lumen seen on MRCP
sequence (arrowhead).

© Radiology and Imaging, Clinical Insitute of Fundeni - Bucharest/RO

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Fig. 20: Calcifying chronic pancreatitis: multiple nodular calcifications involving the
pancreatic tissue (long arrows); segmental dilatations of the MPD, hypotrophy of the
pancreatic body and tail regions

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 21: Obstructive chronic pancreatitis: enhanced CT evaluation- hypertrophy of the
pancreatic head (long arrows), biliary tree dilatation (black arrow head), Wirsung duct
dilatation, pancreatic calcifications, small cysts; note the penetrating duct sign into the
inflammatory mass.

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 22: Obstructive chronic pancreatitis: MRI evaluation using ssFSE short TE and
ssFSE long TE- inflammatory mass involving the head of the pancreas (long arrow)
with positive double duct sign (important dilatation of the main pancreatic duct and the
choledoc), dilatation of the biliary tree (double arrowhead); note the presence into the
pancreatic nodule of millimetric cystic images suggestive for the penetrating duct sign,
histopathological confirmed.

© Lupescu I. et al. RM hepato-bilio-pancreatica, Ed Universitara Carol Davila, 2003, 190

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Fig. 23: Groove pancreatitis and cystic dystrophy of the duodenum: enhanced CT and
MRI evaluation (T1 FS+Gd, T2, MRCP)- duodenal wall thickening, associated with
conglomerate cysts in the pancreatic head, in the groove and into the duodenal wall
(arrowhead)

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 24: Autoimmune pancreatitis: I MRI evaluation T2 FS and T1 FS wi before and
after Gd injection: dffuse enlargement of the pancreatic parenchyma'sausage' like gland,
loss of fatty lobulation. associate with "halo" sign (T2 hypersignal around the pancreatic
parenchyma); important mass effect on the mesenteric vessels and on the portal vein

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Fig. 25: Autoimmune pancreatitis: compared of the MRI findings before and after steroids
treatment-on the I MR evaluation T1 wi after Gd injection there is a major narrowing of
the superior mesenteric vein, splenic vein and the proximal part of the portal vein due to
the diffuse pancreatic enlargement; on the II MR examination (3 months after the I MR),
after steroids treatment, on note the moderate regression of the abnormalities shown on
the I MR.

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Fig. 26: Autoimmune pancreatitis: III-MRI evaluation (T2 wi, T1 FS+Gd) after three years:
appearance of retroperitoneal fibrosis ( black arrows)around the inferior vena cava and
the infrarenal part of the abdominal aorta; hypotrophy of the pancreatic parenchyma

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 27: Pseudocyst of the pancreatic head (arrows)- enhanced CT evaluation:
encapsulated (by a fibrous tissue) fluid collection (arrows)

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Fig. 28: Multiple pancreatic pseudocysts (arrows) located in the pararenal anterior space
(in retrogastric position) and between the duodenum and the pancreatic parenchyma;
important ascites

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Fig. 29: Multiple hemorrhagic pseudocysts (long arrows)- enhanced CT evaluation:
pseudocysts are located in the head of the pancreas with mass effect on the portal vein
(arrowhead) and in the anterior pararenal space; ascites; note the mass effect on the
portal vein trunk (arrowhead)

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Fig. 30: Pseudotumoral chronic pancreatitis involving the pancreatic head with biliary
obstruction, dilatation of main pancreatic duct and pancreatic atrophy (body and tail);
histopathology specimen (van Gieson coloration, x100- Dr.Vlad Herlea)

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Fig. 31: Chronic pancreatitis with acute intramesenteric inflammation (arrow head)fluid
and hemorrhagic collections and superior mesenteric vein thrombosis (long arrow)- MRI
T1FS+Gd evaluation.

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Fig. 32: Arterialised pancreatic pseudocyst (pseudoaneurysm)in a alcoholic patient. I
CT examination: signs of chronic pancreatitis-small pseudocyst of the pancreatic isthmic
region, calcifications. The II unenhanced and enhanced CT evaluation after 2 years: huge
heterogenous encapsulated collection located into the pancreatic head area with cranial
evolution in the hepatic pedicle, that centraly enhance simultaneously with the arterial
abdominal vessels, communicating with the gastroduodenal artery.

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Fig. 33: Pancreatic head adenocarcinoma (T) with dudenal wall invasion and the double
duct sign positive- MRI evaluation T1 FS+Gd in axial abd coronal plane and MRCP

© Lupescu I. et al. RM hepato-bilio-pancreatica, Ed Universitara Carol Davila, 2003, 167

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Fig. 34: Intraductal papillary mucinous tumor: branch type: "polycystic" mass located into
the uncinate process and diffusse and unequel dilatation of the main pancreatic duct with
atrophy of the pancreatic parenchyma

© Lupescu I. et al. RM hepato-bilio-pancreatica, Ed Universitara Carol Davila, 2003, 208

Fig. 35: Acute pancreatitis: MRI T1w evaluation before and after contrast injection:
multiple encapsulated fluid collection into the mesenteric root(arrows); discrete
enlargement of the pancreatic parenchyma

© Radiology and Medical Imaging Department of Fundeni Clinical Institute

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Fig. 36: Typical CT aspects of chronic pancreatitis: atrophy, moniliform dilatation of the
main pancreatic duct, calcifications

© Radiology and Medical Imaging Department Fundeni Clinical Institute

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Fig. 37: Pancreatic pseudocysts (arrow) communicating with the main pancreatic duct
(arrow head)and discrete biliary tree obstruction (black arrow head)

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Fig. 38: Chronic pancreatitis with focal inflammation involving the head of the pancreas;
small pseudoaneurysm of the gastroduodenal artery(arrow); main pancreatic duct
dilatation visualized in the pancreatic body and tail region

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Fig. 39: Cystic dystrophy of the duodenal wall-MRI(MRCP, T1 FS+ Gd in coronal
and axial plane, T2wi)and unenhanced CT evaluation: conglomerate cysts (arrows)
insinuated between the pancreatic head and the medial wall of the duodenum; note the
presence of small calcifications in the pancreatic head parenchyma at the CT exam

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Fig. 40: Chronic pancreatitis with the positive double duct sign (arrows). Others incidenal
findings: huge hepatic encapsulated tumor (adenoma) and fusifom partially thrombosed
aneurysm involving the right common iliac artery; gallbladder microlithiasis (arrow head)

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Conclusion

1.A correct CT and /or MRI protocol evaluation of the pancreas, with a systematic
analysis of the pancreatic tissue, Wirsung duct and adjacent structures, in a strong clinical
suspicion of chronic pancreatitis, in most cases allow the diagnosis of CP.

2.Unequal dilatation of the main pancreatic duct associated with intraductal calculi, cyst
and pseudocyst and pancreatic tissue atrophy are the characteristic signs for chronic
pancreatitis.

3.In pseudotumoral forms of chronic pancreatitis, MRI can bring arguments in favor of a
CP by demonstrating on MRCP the penetrating duct sign.

4.In uncertain cases when imaging is unable to distinguish chronic pancreatitis with a
focal mass from pancreatic adenocarcinoma biopsy and or surgery ar required.

5.Diagnostic cheklist is mandatory to differentiate chronic pancreatitis from others

conditions witch can cause main pancreatic duct dilatation and parenchymal pancreatic
atrophy.

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Personal Information

Assoc.Prof.Dr.Ioana Lupescu

email: ilupescu@gmail.com

Radiology and Medical Imaging Department of Fundeni Clinical Institute

University of Medicine an Pharmacy "Carol Davila" Bucharest

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