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JBR–BTR, 2002, 85: 304-310.
Pancreatitis is the most common
benign disease involving the pan-
creas. Pancreatitis is classified as
acute or chronic on the basis of clini-
cal, morphologic, and histologic cri-
teria. Chronic pancreatitis (CP) is a
chronic clinical disorder pathologi-
cally characterized by loss of exo-
crine and endocrine pancreatic
parenchyma, irregular fibrosis, cel-
lular infiltration, and ductal abnor-
malities. In general, these lesions
show irregular, patchy distribution
with variable intensities in the
whole pancreas, they do not resol-
ve, and show various levels of dete-
rioration. Typically, the first clinical
manifestations consist of abdominal
pain and tenderness. With further
disease progression, symptoms of
exocrine and endocrine pancreatic
insufficiency may occur.
CP is usually classified according
to etiology into alcoholic pancreati-
tis, nonalcoholic duct-destructive
CP, biliary pancreatitis, CP due to
less common etiologies (hereditary,
hyperparathyroidism, autoimmune
diseases, etc.), groove pancreatitis,
and idiopathic pancreatitis.
Diagnostic role of CT and MRI
Replacement of glandular acini,
their ducts, and their blood vessels
by fibrous tissue in CP results in
duct strictures with upstream dilata-
tion, stasis and subsequent paren-
chymal atrophy and calculi forma-
tion. Local or branch duct obstruc-
tions may cause focal or diffuse
inflammatory enlargement.
CT and MRI findings consistent
with CP are dilatation of the main
pancreatic duct and its side branch-
es, irregularities in duct caliber, atro-
phy of the pancreas, and pancreatic
calcification (Fig. 1). Size alone is
not specific for chronic pancreatitis.
During and immediately after an
acute relapse of pancreatitis, the
pancreas may be enlarged, but in
more advanced cases, the pancreas
atrophies and is small. Additional,
but less common, radiographic find-
ings include smooth and tapered
strictures of the intrapancreatic por-
tion of the common bile duct with
mild to moderate dilatation of the
suprapancreatic bile duct, pancreat-
ic fluid collections, focal or diffuse
REVIEW ARTICLE
CHRONIC PANCREATITIS: DIAGNOSTIC ROLE OF COMPUTED TOMOGRA-
PHY AND MAGNETIC RESONANCE IMAGING
A.I. De Backer
1
, K.J. Mortelé
2
, P.R. Ros
2
, D. Vanbeckevoort
3
, I. Vanschoubroeck
4
, B. De Keulenaer
4
The value of computed tomography (CT) and magnetic resonance imaging (MRI) in the diagnosis and detection of
complications in patients with chronic pancreatitis are reviewed. CT and MRI diagnoses are based on changes in the
pancreatic duct and parenchyma and on the detection of ductal calculi. Despite technical refinements of these imag-
ing methods, the diagnosis of chronic pancreatitis remains often difficult because of the complexity of the mor-
phologic changes and the false-negative results in the early stages of the disease.
This article describes and illustrates the imaging features of chronic pancreatitis classified according to the under-
lying etiology.
Key-words: Pancreatitis – Pancreas, CT – Pancreas, MR.
From: Department of 1. Radiology and 4. Internal Medicine, Algemeen Centrumzieken-
huis Antwerpen, Campus Stuivenberg, Antwerpen, Belgium, 2. Department of Radio-
logy, Abdominal Imaging Group, Brigham and Women’s Hospital, Boston, USA,
3. Department of Radiology, University Hospitals Katholieke Universiteit Leuven,
Leuven, Belgium.
Address for correspondence: Dr A.I. De Backer, Dpt of Radiology, Algemeen Centrum-
ziekenhuis Antwerpen, Campus Stuivenberg, Lange Beeldekensstraat 267,
B-2060 Antwerpen, Belgium.
Fig. 1. — Chronic pancreatitis in a 54-year-old alcoholic man with chronic, episodic
abdominal pain. Contrast-enhanced CT shows atrophy of the pancreas and irregulari-
ty of the main pancreatic duct. Calculi are seen in the main pancreatic duct.
CHRONIC PANCREATITIS: DIAGNOSTIC ROLE OF CT AND MRI — A.I. DE BACKER et al 305
enlargement of the pancreas, alter-
ations in peripancreatic fat or perire-
nal fascia, splenic vein occlusion,
and peripancreatic pseudoa-
neurysm (1, 2).
Pancreatic duct dilatation, paren-
chymal atrophy, enlargement or
focal masses, chronic pseudocysts,
and vascular complications may be
detected easily both on CT and MRI.
Small calculi are demonstrated
more reliably on CT, especially on
unenhanced images. Contrary to
advanced CP, early diagnosis based
on morphologic changes using CT
and MRI remains contentious and
diagnosis of early stages of CP is
entirely dependent on endoscopic
retrograde cholangiopancreatogra-
phy (ERCP). The morphologic classi-
fication proposed at the internation-
al workshop of Cambridge classifies
the severity of ductal changes as
equivocal, mild, moderate, or
marked (3). ERCP is, at present, the
most sensitive diagnostic method
for evaluation of early changes in
the main pancreatic duct and its side
branches. This characteristic prun-
ing or irregularity of side branch
ducts are not accurately demon-
strated by CT or MRI techniques.
Magnetic resonance cholangio-
pancreatography (MRCP) has
become an important noninvasive
diagnostic procedure in the evalua-
tion of pancreatic ductal abnormali-
ties and carries no risk of complica-
tions. A limitation of MRCP is the
difficulty to visualize the side
branches and tail of the pancreas.
Minimally dilated side branches are
not routinely recognized, leading to
a high false-negative rate in diag-
nosing mild pancreatitis (4).
Stimulating pancreatic juice output
with intravenous secretin, with a
consequent increase in volume of
fluids inside the pancreatic ducts,
has been shown to improve the
delineation of the pancreatic ducts
and the possibility of sequential
acquisitions after secretin adminis-
tration has been proposed to
increase the diagnostic confidence
of interpretation of ductal abnormal-
ities (5, 6). To date, the role of MRCP
is limited to the diagnosis and fol-
low-up of advanced cases. Criteria
for diagnosing chronic pancreatitis
consist of irregular dilatation with a
beaded appearance (alternation of
dilated and stenotic segments) of
the pancreatic duct, filling defects
within the pancreatic duct (calculi,
proteinaceous plaques or mucinous
casts), pseudocysts, and a tapered
stricture of the common bile duct.
With further improvement of imag-
ing technique, MRCP may probably
become a valid, noninvasive alterna-
tive to diagnostic ERCP in patients
with mild pancreatic disease.
The attenuation of abnormal pan-
creatic tissue remains normal on CT,
even in advanced disease. However,
in some patients with advanced dis-
ease the alterations caused by fibro-
sis and inflammatory infiltrates may
be visualized as inhomogeneous
enhancement of the pancreas with
areas of normal enhancement inter-
spersed within areas of decreased
enhancement (1, 7) (Fig. 2).
Characteristic MRI signal changes
occur with established disease.
Pancreatic parenchyma shows
diminished signal intensity on T1-
weighted images, especially evident
with the use of fat suppression tech-
niques (8). The decreased signal
intensity on T1-weighted fat-sup-
pressed images reflects the loss of
soluble proteins in the acini of the
pancreas secondary to fibrosis (9).
On T2-weighted images, the signal
intensity of the pancreas is variable
and may be normal because of the
presence of fibrous tissue with vari-
able degrees of inflammation and
residual pancreatic tissue (10). In
patients with significant fibrosis,
probably because of the obliteration
of small vessels by fibrosis, paren-
chymal enhancement with Gd-DTPA
is both less intense and more grad-
ual than in the normal pancreas (8,
11) (Fig. 3a-c). Lower enhancement
of pancreatic parenchyma has been
reported in patients with chronic
pancreatitis and calcification, com-
pared with that in patients with
chronic pancreatitis without calcifi-
cation (8). In focal pancreatitis,
affected areas enhance more slowly
than normal pancreatic parenchyma
(10). Calcifications appear as areas
of signal void on both T1- and T2-
weighted images. Tiny cysts or
pseudocysts within the pancreas
will be differentiated from calculi
based on their high signal intensity
on T2-weighted images (1).
Differentiation inflammatory mass
from carcinoma
Areas of focal enlargement within
the pancreas representing inflam-
matory masses may arise in both
early and advanced stages of CP.
Malignant masses arise relatively
uncommonly in CP, but when pre-
sent, differentiation with these
benign lesions may be very difficult.
Both types of lesions occur most
often in the pancreatic head, may
cause bile duct obstruction, and
may present in the absence of calci-
fication or duct strictures and dilata-
tion. However, patients with an
inflammatory mass are likely to be
younger at the time of presentation,
have a history of alcoholism and
have a history of previous episodes
of acute or CP (1). Patients with bil-
iary tract obstruction due to pancre-
atitis usually have a history of
abdominal and back pain preceding
Fig. 2. — CT findings in advanced chronic pancreatitis. An inhomogeneous enhance-
ment of the pancreatic head is seen. Note also the presence of calcifications.
306 JBR–BTR, 2002, 85 (6)
the onset of jaundice. Jaundice due
to pancreatitis often fluctuates in
contrast to the continuously pro-
gressive jaundice found in patients
with pancreatic carcinoma. The
serum concentration of total biliru-
bin level is usually much higher in
patients with pancreatic carcinoma
than in those with chronic pancreati-
tis (12).
On unenhanced CT, both inflam-
matory masses and small carcino-
mas are usually iso-dense with nor-
mal pancreatic tissue and, when
located in the pancreatic head, may
cause upstream dilatation of the
duct and atrophy of the tail.
Carcinoma is typically hypovascular
and seen as a low density mass sur-
rounded by normal parenchyma.
Sometimes, inflammatory tissue
caused by obstructive pancreatitis
may surround the tumor, resulting
in peripheral enhancement. Tumor
obstruction of the main pancreatic
duct may lead to rupture of a side
branch resulting in pseudocysts.
Inflammatory masses may also
show reduced contrast enhance-
ment. However, this reduction is
less marked than in the typical carci-
noma.
On T1-weighted fat suppressed
images, areas of chronic pancreati-
tis show diminished signal intensity
compared with normal pancreas,
but the degree of signal reduction is
usually less than that associated
with carcinoma. On this sequence,
normal pancreatic tissue shows sig-
nal intensities markedly higher than
normal liver parenchyma. Inflam-
matory masses in CP may result in
signal intensities comparable with
that of the liver, whereas carcinoma
often shows signal intensities hypo-
intense to the liver (9). Small areas
of low signal intensity may be pre-
sent in an inflammatory mass and
represent small pseudocysts or cal-
cifications. With carcinoma, the pan-
creas distal to the mass lesion has
usually normal signal intensity on
both T1-weighted fat-suppressed
and dynamic contrast-enhanced
images. However, chronic obstruc-
tion of the main pancreatic duct may
result in CP distal to the mass lesion.
The latter is usually seen in large
carcinoma and is often easily diag-
nosed. Occasionally, however, small
carcinoma may be associated with
distal CP (9). When present, MRI and
CT may fail to differentiate these
small carcinomas from CP requiring
further diagnostic work-up.
Evaluating the main pancreatic
duct using MRCP has been reported
to be helpful, owing to its sufficient-
ly high sensitivity and specificity for
distinguishing inflammatory pan-
creatic mass from pancreatic carci-
noma (13). The duct-penetrating
sign on MRCP images – a smoothly
stenotic or normal main pancreatic
duct penetrating into a mass - has
been reported to occur more fre-
quently in inflammatory pancreatic
mass than in pancreatic carcinoma.
Especially, if the duct-penetrating
sign was considered to be a normal
main pancreatic duct penetrating a
mass, the specificity for inflammato-
ry pancreatic mass has been report-
ed to be 100% (13).
The relation between acute and
chronic pancreatitis
Acute and chronic pancreatitis
are thought to be different diseases
and only rarely does acute pancre-
atitis lead to CP. Most cases of true
acute pancreatitis, such as recurrent
bouts of acute pancreatitis sec-
ondary to biliary disease, do not
result in CP. However, in patients
with chronic alcohol abuse associat-
ed with asymptomatic, substantial
and diffuse pancreatic fibrosis, the
initial bout of clinical pancreatitis
heralds the onset of chronic pancre-
atitis. In alcoholics a strong associa-
tion with CP has been reported (14-
16).
Fig. 3. — MRI findings in advanced chronic pancreatitis.
A: T1–weighted GRE image with fat suppression shows pancre-
atic head as hypointense. B: On the arterial-phase contrast-
enhanced dynamic GRE image with fat suppression, the pan-
creatic head shows a less intense enhancement. C: On the por-
tal-phase, decreased enhancement with heterogeneity is seen.
B
C
A
CHRONIC PANCREATITIS: DIAGNOSTIC ROLE OF CT AND MRI — A.I. DE BACKER et al 307
Fig. 4. — Segmental form of groove pancreatitis. A: Contrast-enhanced CT image shows a hypodense mass between the head of
the pancreas and the duodenun. The lesion causes duodenal stenosis and obstruction of the main pancreatic duct with dilatation.
B: Axial and C: coronal fat-suppressed fast-spin-echo T2-weighted images show not only cystic lesions between the head of the
pancreas and the duodenum, but also in the wall of the duodenum. D: MR cholangiopancreatography demonstrates a long
segmental smooth stenosis of the common bile duct and a stricture of the main pancreatic duct with upstream dilatation. Cysts
within the groove and the duodenal wall also are demonstrated.
B
CD
A
Fig. 5. — Alcoholic chronic pancreatitis. A: A markedly dilated pancreatic duct and multiple calcifications are seen in a patient in
whom there was long standing alcohol abuse. A pseudocyst is visible in the tail of the pancreas. B: Axial fat-suppressed fast-spin-
echo T2-weighted image shows ectasia and irregularity of the main pancreatic duct and its side branches containing calculi.
B
A
308 JBR–BTR, 2002, 85 (6)
Groove pancreatitis
Groove pancreatitis is an uncom-
mon type of chronic pancreatitis
localized within the “groove”
between the head of the pancreas,
the duodenum, and the common
bile duct (17). The pathogenesis
remains unclear, although several
factors, such as penetrating duode-
nal ulcers, trauma to the head of the
pancreas after gastric resections,
true duodenal wall or pancreatic
cysts, pancreatic heterotopia in the
duodenum, microscopic carcinoma
obstructing Santorini’s duct, and
disturbance of flow of pancreatic
juice in the Santorini duct, might be
related to this condition (18, 19). A
long history of alcohol abuse is
often found in patients presenting
with groove pancreatitis (20).
Groove pancreatitis is classified
into two types, the pure form and
the segmental form (17). The pure
form affects the groove only, while
the pancreatic parenchyma is pre-
served; the pancreatic duct is intact
and the condition is seldom detect-
ed. In segmental groove pancreati-
Fig. 6. — Autoimmune pancreatitis. A: Helical CT shows dif-
fuse pancreatic enlargement. B: T1-weighted MR image shows
pancreatic body and tail as hypointense. C: T2-weighted fat-
suppressed MR image shows pancreatic parenchyma as hyper-
intense. On gadolinium-enhanced T1–weighted GRE images
with fat suppression (D) decreased contrast enhancement is
seen on the arterial phase and, (E) normal enhancement on the
delayed-phase.
B
C
D
E
A
CHRONIC PANCREATITIS: DIAGNOSTIC ROLE OF CT AND MRI — A.I. DE BACKER et al 309
Fig. 7. — Small adenocarcinoma of the pancreas. Atrophy of
the tail of pancreas with dilated pancreatic duct is noted. The
small carcinoma in the body of the pancreas was not seen on
CT and CT-guided percutaneous biopsy was negative. Surgery
confirmed a small carcinoma.
tis, scarring is found not only in the
groove but also in the pancreatic
parenchyma. The replacement of
parenchyma by scar tissue is
extended to the dorso-cranial por-
tion of the pancreatic head.
Segmental groove pancreatitis often
shows stenosis or obstruction of
Santorini’s duct, while preserving
Wirsung’s duct.
On dynamic CT, the cicatricial
“plate” in the “groove” may present
as a mass lesion with poor enhance-
ment and may resemble carcinoma
of the head of the pancreas.
Additional findings may consist of
cysts in the duodenal wall and/or
the groove, and duodenal wall thick-
ening often accompanied by duode-
nal stenosis. In segmental groove
pancreatitis a long, smooth stenosis
of the distal common bile duct has
also been reported (17).
The most characteristic MRI find-
ing in groove pancreatitis is a sheet-
like mass between the head of the
pancreas and the thickened duode-
nal wall. The mass shows hypo-
intensity relatively to pancreatic
parenchyma on T1-weighted
images, iso or slightly hyperintensi-
ty on T2-weighted images, and
delayed contrast enhancement on
the late-phase images after injection
of contrast material, reflecting the
fibrotic changes of this scarring
mass (18). Cysts, either true cysts or
pseudocysts, may be present in the
groove and/or in the duodenal wall
and may be easily detected on T2-
weighted images (Fig. 4A-C).
Alcoholic chronic pancreatitis
In Western countries, alcohol
abuse is responsible for approxi-
mately 70% of cases of CP. Sub-
stantial pancreatic fibrosis has been
reported at autopsy in 50% of chron-
ic alcoholics who did not have clini-
cal CP. Despite that impressive num-
ber, only 5% to 15% of alcoholics
develop clinical CP (21). These data
suggest that alcohol produces pan-
creatic injury in many or most peo-
ple who drink alcohol to the point of
abuse. However, most do not pass
the clinical threshold for the diagno-
sis of CP.
Classically, in alcoholic CP, the
ducts are distorted and often con-
tain calcifications (Fig. 5A-C). Pan-
creatic calcifications have been
reported to occur more frequently in
substantial pancreatic fibrosis while
the absence of calcifications
denotes less severe disease. In the
initial phase of alcoholic CP, protein
precipitates are deposited in the
acini and pancreatic ducts, which
subsequently undergo calcification
to a variable extent. Therefore, not
all patients with pancreatic fibrosis
will have pancreatic calcifica-
tions (22). In hereditary pancreatitis,
calcifications occur early in the
course of the disease and tend to be
large and to arrange themselves in a
linear fashion within the main pan-
creatic duct (23).
When alcoholic CP occurs in
patients with pancreas divisum, iso-
lated ductal alterations involving the
ventral or dorsal pancreas may be
seen as the first manifestation of a
generalized pancreatic disease (24).
This finding could be related to local
ductal hypertension arising earlier
either in the ventral or the dorsal
duct. Finally, with further disease
progression, involvement of both
ducts is normally seen.
Autoimmune pancreatitis
Autoimmune pancreatitis is
defined as a special form of CP
caused by an autoimmune mecha-
nism. Associated autoimmune and
related diseases have been reported
in about 50% of cases and may be
the key to a correct diagnosis.
Associations with Sjögren’s syn-
drome, primary sclerosing cholangi-
tis, primary biliary cirrhosis, inflam-
matory bowel disease, and systemic
lupus erythematosus have been
described (25). Typical laboratory
findings in autoimmune pancreatitis
include increased serum gamma-
globulin and IgG and the presence
of autoantibodies (26). Clinical
characteristics of autoimmune pan-
creatitis include mild symptoms
without acute attacks of pancreati-
tis, no association with alcohol
abuse, high incidence of obstructive
jaundice and diabetes mellitus, and
effective clinical response to steroid
therapy. Specific histopathologic
features of autoimmune pancreatitis
include massive fibrosis, marked
destruction of pancreatic islets and
acini, and periductal lymphocytic
infiltration causing narrowing
and/or destruction of the main pan-
creatic duct and/or its side branches
and fibrosis. Based on this histolog-
ical aspect, the disease has also
been called nonalcoholic duct-
destructive chronic pancreatitis (27).
Characteristic CT and MRI fea-
tures of autoimmune or nonalco-
holic duct-destructive CP include dif-
fuse or focal pancreatic enlarge-
ment, narrowing of the main pancre-
atic duct, decreased signal intensity
on T1-weighted MR images and
increased signal intensity on T2-
weighted images. Additionally, con-
trast-enhanced imaging may show a
capsular-like rim, decreased enhan-
cement on the arterial-phase imag-
es, and normal enhancement on the
delayed-phase images (Fig. 6A-E).
On CT, this capsular-like rim is seen
as a well-defined low-density band
surrounding the pancreas (25, 26,
28). Recognition of autoimmune
pancreatitis is clinically important
because it is reversible when diag-
nosed and treated correctly.
310 JBR–BTR, 2002, 85 (6)
Chronic obstructive pancreatitis
Chronic obstructive pancreatitis
results from obstruction of the pan-
creatic ducts, most frequently occur-
ring distally to a pancreatic neo-
plasm. Narrowing or obstruction of
the main pancreatic duct involved
by carcinoma of the pancreatic head
is characterized by dilatation of the
distal main pancreatic duct and
parenchymal atrophy, and seldom
leads to dilatation of the duct of
Santorini. The lesions are regularly
spread in the occluded territory, pro-
tein plugs are rare, and calcifica-
tions are not observed. On T1-
weighted fat suppressed dynamic
contrast-enhanced images, chronic
obstructive pancreatitis will show
slightly increased contrast enhance-
ment compared to the low signal-
intensity carcinoma. However,
sometimes, chronic obstructive pan-
creatitis may be a diagnostic clue to
small pancreatic carcinoma (Fig. 7).
In patients undergoing pancreatoje-
junostomy for drainage of chronic
pancreatitis the occurrence of
unsuspected carcinoma with fatal
outcome has been reported (29-31).
Of the 16 small carcinomas reported
by Moosa and Levin (32), 4 were
incidentally found by microscopy
examination of the specimen resect-
ed with a presumptive diagnosis of
chronic pancreatitis. The frequency
of chronic pancreatitis-associated
pancreatic carcinoma, the diagnos-
tic difficulty involved, and the very
short survival of patients with pan-
creatic carcinoma justifies a con-
scientious follow-up or, in doubtful
cases, further diagnostic work-up.
Needle biopsy is helpful if it shows
malignant disease, but the discov-
ery of inflammatory histology may
raise the suspicion that the lesion
has been missed. Surgical inspec-
tion at laparotomy is usually unable
to differentiate benign from malig-
nant masses when the lesion is well
localised (33).
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