R e s i d e n t s S e c t i o n S t r u c t u r e d R ev i ew A r t i c l e

OConnor et al.
Imaging of Acute Pancreatitis

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Residents Section
Structured Review Article

Residents

inRadiology
Owen J. OConnor 1
Sebastian McWilliams1
Michael M. Maher 1,2
OConnor OJ, McWilliams S, Maher MM

Imaging of Acute Pancreatitis

Educational Objectives
1. Acute pancreatitis is an acute inflammatory process of the pancreas that may also in
volve adjacent or remote tissues and organs.
2. Imaging is frequently recommended to confirm the clinical diagnosis, ascertain the
cause, and grade the extent and severity of acute pancreatitis.
3. Radiography, upper gastrointestinal series, and ultrasound are of limited value in the di
agnosis of acute pancreatitis.
4. CT currently plays an important role in imaging of patients with acute pancreatitis, the
identification of complications, and assessing the response to treatment.
5. Although sensitive for the detection of acute pancreatitis, MRI is used less commonly than
CT. MRI is especially useful for imaging patients with iodine allergies, characterizing collections,
and evaluation of an abnormal or disconnected pancreatic duct that is easily overlooked. In ad
dition, a heavily T2-weighted MRCP sequence may assist in diagnosis of choledocholithiasis.

Keywords: acute pancreatitis, CT abdomen, CT severity

index, pancreatic pseudocyst
DOI:10.2214/AJR.10.4338
Received January 26, 2010; accepted after revision
July12, 2010.
1

Department of Radiology, Cork University Hospital,

University College Cork, Wilton, Cork, Ireland. Address
correspondence to M. M. Maher (m.maher@ucc.ie).
2
Department of Radiology, Mercy University Hospital,
Cork, Ireland.

WEB
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American Roentgen Ray Society

cute pancreatitis is an important

cause of acute abdominal pain.
Imaging plays a central role in
the management of selected cas
es of acute pancreatitis, complementing lab
oratory investigations such as serum amylase
and lipase levels that have relatively high
sensitivity and specificity. In addition to clin
ical signs and laboratory investigations, im
aging helps confirm the clinical diagnosis
when there is uncertainty and elucidate the
cause and grade the extent and severity of
acute pancreatitis. Imaging also aids in the
early detection of complications [1].
Pathophysiologic Basis
Acute pancreatitis is an acute inflammato
ry process of the pancreas that may involve
adjacent or remote tissues and organs [2]. The
causes of acute pancreatitis are protean (Ta
ble 1), with gallstones and alcohol responsible
for approximately 90% of cases in the United
States [1, 3] (Fig. 1). In practice, serum amy
lase or lipase levels greater than three times
normal are used to confirm acute pancreatitis
[4]. Acute pancreatitis may be classified based
on clinical, morphologic, or histologic criteria
and many systems of classification exist, most
based on the cause or severity [1, 2, 5].

Grading of Disease Severity

The severity of acute pancreatitis may
be broadly subdivided into mild and severe
forms. Patients with mild acute pancreatit
is tend to have acute interstitial pancreatit
is whereas pancreatitis associated with hem
orrhage, necrosis, or vasculitis is considered
severe [6]. Most cases of acute pancreatitis
are considered mild, with affected patients
reporting modest abdominal pain and dis
playing mild abdominal tenderness. Patients
with mild acute pancreatitis have either min
imal or no organ and systemic dysfunction.
Therefore, patients with mild acute pancrea
titis should respond quickly to medical ther
apy, and their symptoms and laboratory val
ues should normalize promptly [2].
Between 10% and 20% of cases of acute
pancreatitis are considered severe [7]. Such
patients will usually exhibit more severe ab
dominal pain, vomiting, and clinical signs of
peritonism with tachycardia, fever, and leu
kocytosis. Patients with severe acute pancre
atitis are more likely to have a protracted hos
pital stay and to develop systemic or organ
failure with renal, respiratory, and cardio
vascular failure; disseminated intravascular
coagulation; or gastrointestinal hemorrhage
[2]. The clinical evaluation of severe acute

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OConnor et al.
pancreatitis is unreliable. It is estimated that
experienced clinicians predict which pa
tients will develop severe acute pancreati
tis in less than 40% of cases [8]. Examples
of clinical systems that have been developed
to more accurately and reproducibly grade
the severity of acute pancreatitis include the
Acute Physiology and Chronic Health Evalu
ation II (APACHE II), Ransons criteria, and
the Glasgow original and modified systems
[9, 10]. A Ransons score of 3 or more and
an APACHE score of 8 or more suggest the
presence of severe acute pancreatitis [10].
Scoring systems also help predict the likely
course of acute pancreatitis at the time of pre
sentation. This helps guide treatment-related
decision making, such as the necessity for ad
mission into an ICU or transfer to a tertiary
referral center [3]. The sensitivity and speci
ficity of the APACHE II system for assessing
severe acute pancreatitis at the time of admis
sion are 75% and 79%, respectively [11]. Clin
ical grading systems, such as the APACHE II
system, indirectly estimate the degree of pan
creatic damage. To directly evaluate and es
timate the degree of parenchymal injury and
to improve the early prognostic value of CT
in acute pancreatitis, the CT severity index
(CTSI) was developed [11]. The CTSI grades
acute pancreatitis into five levels of increasing
severity (A to E) using a 10-point scale. Points
are awarded on the basis of the presence of
pancreatic enlargement, fat stranding, and flu
id collections and the amount of pancreatic
necrosis. The CTSI is discussed in more de
tail in the systematic review of the complica
tions of acute pancreatitis in an upcoming is
sue of the AJR.
A new subgroup of acute pancreatitis has
recently been described, termed moderate
ly severe acute pancreatitis, consisting of
patients with local complications similar to
those with severe acute pancreatitis but low
er morbidity, which is believed to be due to
more transient organ dysfunction [12].
Disease Epidemiology
The incidence of acute pancreatitis is ap
proximately 570 cases per 100,000 per year
[13, 14]. Gallstones and alcohol are respon
sible for approximately 70% of cases [15].
Among patients with gallstones, acute pancre
atitis has a higher incidence in men than wom
en, but overall, gallstone acute pancreatitis is
most frequent in women (generally between
40 and 50 years old) [16]. Gallstones and al
cohol have been implicated in the develop
ment of recurrent attacks of acute pancreati

W222

TABLE 1: Causes of Acute Pancreatitis

Type

Causes

Mechanical

Cholelithiasis; postoperative, ERCP, blunt, or penetrating trauma; anatomic variants

(pancreas divisum, choledochocele, perivaterian duodenal diverticulum)

Metabolic

Alcohol, hyperlipidemia, hypercalcemia, hereditary, scorpion venom

Drugs

Corticosteroids, azathioprine, 6-mercaptopurine, thiazide diuretics, furosemide,

aminosalicylic acid, sulfonamides, tetracycline, procainamide, and opiates

Infections

Measles, mumps, AIDS or HIV, cytomegalovirus, fungi (Aspergillus), and parasites

(Toxoplasma)

Vascular

Polyarteritis nodosa, atheroembolism, and after abdominal and cardiac surgery

Idiopathic

Biliary sludge, microlithiasis, congenital

tis. Interestingly, it has been observed in one

cohort that only alcoholic patients progressed
from acute to chronic pancreatitis [17]. In
this group, a second attack of acute pancre
atitis was associated with a 38% incidence
of chronic pancreatitis [17]. The incidence of
acute pancreatitis is increasing, and a 100%
increase in the number of hospitalizations
over the past two decades has been recorded

in the United States [18]. This trend is pos

sibly secondary to the increasing age of the
population and increasing alcohol consump
tion, but mortality rates appear stable [14].

Indications for Imaging

The clinical signs of acute pancreatitis are
nonspecific, with serum amylase and lipase
levels correlating poorly with disease severity

Fig. 1CT in 54-year-old man with abdominal pain and raised serum amylase 3 days after blunt abdominal
trauma.
A and B, CT images show disruption and discontinuity of pancreatic neck (arrow, A) and extensive stranding of
retroperitoneal and intraperitoneal fat (arrowhead, B).

TABLE 2: Indications for CT Imaging in Acute Pancreatitis

Type
Diagnostic CT

Indications
1. When the diagnosis of acute pancreatitis is uncertain
2. Patients with hyperamylasemia, severe clinical pancreatitis, abdominal distention
and tenderness, fever > 102, and leukocytosis for the detection of complications
3. Ranson score > 3 or APACHE score > 8
4. Patients who fail to improve after 72 hours of conservative medical therapy
5. Acute change in clinical status, such as new fever, pain, and shock after
successful initial medical therapy

Delayed CT

1. Changing clinical status suggesting complication

2. 710 days after presentation if CT severity score is 310 at presentation or grade
DE pancreatitis
3. After surgery or interventional radiologic procedures to document response to
treatment
4. Before discharge of patients with severe acute pancreatitis

NoteAPACHE = Acute Physiology and Chronic Health Evaluation.

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Imaging of Acute Pancreatitis

Fig. 2CT of 35-year-old man with acute-on-chronic pancreatitis due to alcohol abuse.
A, Control phase CT image shows several calcifications in head of pancreas (arrowhead) suggesting chronic
pancreatitis.
B, Contrast-enhanced CT image (pancreatic parenchymal phase) shows heterogeneous enhancement of
pancreas, and pancreatic head appears edematous with associated stranding of peripancreatic fat. There are
small peripancreatic fluid collections (acute pancreatic fluid collections) (arrowhead).

[1]. Elevated plasma serum amylase and lipase

levels are not specific to acute pancreatitis
and may be elevated by bowel obstruction,
infarction, cholecystitis, and perforated ul
cer. Imaging is recommended to confirm the
clinical diagnosis, diagnose its cause, ex
clude alternative causes of abdominal pain,
and grade the extent and severity of acute
pancreatitis [1, 13] (Table 2). Follow-up CT
is not considered necessary if the CTSI score
is between 0 and 2 on initial CT [2]. The
British Society of Gastroenterology guide
lines recommend imaging between 3 and 10
days after presentation [19]. Some groups
recommend imaging within 24 hours to
identify the cause of acute pancreatitis be
cause ERCP and sphincterotomy within 72
hours in patients with gallstone-related acute
pancreatitis have been proposed as a treat

Fig. 4CT of 67-year-old woman with mild

acute pancreatitis. Head of pancreas enhances
homogeneously (long arrow) on portal venous
phase imaging. There is extensive stranding of
retroperitoneal fat, and acute fluid collections are
seen in left anterior pararenal space (short arrow).

ment strategy aimed at reducing the chance

of developing severe or complicated acute
pancreatitis [20].
At our institution, a three-phase (control,
pancreatic parenchymal phase (40 seconds),
and portal venous phase) protocol with pos
itive oral contrast administration is used for
the initial assessment of acute pancreatitis
(Fig. 2). The pancreatic parenchymal phase
is the optimal phase for assessment for necro
sis because normal pancreatic tissue enhanc
es greatest during this phase. Subsequent im
aging with CT is generally performed using
a single-phase technique in the portal venous
phase. Many variations in CT technique ex
ist. A dual-phase technique (pancreatic and
portal venous phases) is commonly used but
risks missing hemorrhagic collections [21]. It
is also recommended that thin-slice (3 mm)

Fig. 5CT image of abdomen of 67-year-old man

with acute pancreatitis and acute hemorrhagic
pancreatic collection. On unenhanced CT image,
pancreas shows heterogeneous areas of increased
density (arrows), consistent with blood in region of
pancreatic head and tail on this unenhanced study.
Note absence of wall around collection, as seen with
pseudocyst.

Fig. 3Ultrasound of 74-year-old woman with mild

acute pancreatitis. Pancreatic body and tail are
hypoechoic due to edema anterior to pancreatic duct
(arrow).

CT should be used for imaging the pancreas;

this may be of particular benefit for the plan
ning of operative intervention [21]. The use of
positive oral contrast material may mask hem
orrhage or calculi, and for this reason many
institutions use negative oral contrast materi
al. The suggestion that IV administration of
iodinated contrast material can increase the
severity and duration of acute pancreatitis has
led to conflicting opinions regarding IV con
trast usage, and at present the benefits of IV
contrast administration appear to outweigh
the potential risks [22, 23]. MRI is compara
ble with CT for the assessment of acute pan
creatitis [24]. In practice, MRI is particularly
useful for the imaging of patients with iodine
allergies; for the characterization of collec
tions in cases in which there is diagnostic un
certainty; and for evaluating the biliary tract,
including the bile ducts and pancreatic duct.
Imaging Appearances
Conventional radiography and upper gas
trointestinal series no longer play an important
role in the diagnosis of acute pancreatitis. Ra
diographic signs of acute pancreatitis include
the sentinel loop sign (dilated air-filled duode
num or jejunum), the colon cutoff sign (dilat
ed large bowel to the level of the splenic flex
ure), loss of the left psoas shadow, ascites, or
a gasless abdomen [13]. Pleural effusions, at
electasis, or an elevated hemidiaphragm are
suggestive of severe acute pancreatitis [25].
Thickened rugal and duodenal folds, indenta
tion of the stomach, and enlargement of the Cloop of the duodenum are signs of acute pan
creatitis on barium meal and follow-through
studies [13]. Sonography of patients with acute
pancreatitis is often negatively impacted by

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OConnor et al.

Fig. 6CT of 45-year-old man with acute pancreatitis

complicated by necrosis. On CT image, majority of
pancreas fails to enhance apart from small portion
of pancreatic body (arrow). This patient is at risk for
disconnection of pancreatic duct because viable
pancreatic tissue is separated from gastrointestinal
tract by necrotic tissue.

Fig. 7Portal venous phase CT of abdomen of

75-year-old woman with acute pancreatitis who had
profound sepsis. There is hypoattenuating collection
replacing pancreatic neck (arrow) with stranding
of peripancreatic fat. Note thick wall surrounding
collection. Aspiration confirmed this to be abscess.

Fig. 8Fat-suppressed T2-weighted MR image of

41-year-old woman with mild acute pancreatitis.
Pancreas is edematous and enlarged with diffusely
increased signal and loss of normal lobular contour of
body and tail (arrow).

difficulty visualizing the pancreas because of

ileus and overlying bowel gas [10]. Abnormal
ultrasound findings are seen in 3390% of pa
tients with acute pancreatitis [10]. Interstitial
edema in acute pancreatitis is depicted on ul
trasound as an enlarged hypoechoic gland
(Fig. 3). Although ultrasound may be used to
identify peripancreatic acute fluid collections,
it is not useful for the detection of necrosis, and
therefore its main role in the imaging of acute
pancreatitis is limited to the detection of chole
lithiasis and choledocholithiasis and identifi
cation of fluid collections in the peritoneum,
retroperitoneum, and pleural spaces [10].
Contrast-enhanced CT is the imaging mo
dality of choice for the diagnosis and staging
of acute pancreatitis [3, 13]. The pancreas
enhances uniformly in mild acute pancrea
titis and may be normal or enlarged with a
variable amount of increased attenuation in
the adjacent fat, termed stranding [2, 26]
(Fig. 4). Local edema is a common finding
and may extend along the mesentry, meso
colon, and hepatoduodenal ligament and
into peritoneal spaces. Extension of edem
atous fluid into the anterior perirenal space
may create a mass effect and a halo sign with
sparing of the perinephric fat [27].
Peripancreatic fluid collections consist of
exudate, peripancreatic fat tissue necrosis, or
hemorrhage [13] (Fig. 5). An organized peri
pancreatic fluid collection with a fibrous wall
occurring greater than 4 weeks after the on
set of symptoms is termed a pseudocyst [2].
Edema is differentiated from fluid collections
by the identification of fat islands of normal
tissue within edematous fluid [26]. It is usu
ally possible to differentiate acute collections
from necrosis. In cases in which CT is unable
to accurately differentiate peripancreatic fluid
collections from extrapancreatic fat tissue ne

crosis, it is thought to be safer to consider het

erogeneous pancreatic collections as necrotic
until proven otherwise [11]. Nonenhancement
of all or part of the gland is termed necrosis
[19] (Fig. 6). CT is 100% specific for necrosis
if greater than 30% of the gland is nonenhanc
ing [13]. Necrosis develops between 24 and
48 hours after the onset of acute pancreatitis,
and therefore CT within the first 12 hours may
be falsely reassuring [11]. Pancreatic abscess
formation is usually observed 46 weeks af
ter the onset of acute pancreatitis as an area
of low attenuation containing pus and a thick
wall that may enhance after IV contrast ad
ministration [2, 3]. Necrosis and abscess are
considered among the most important imag
ing features of acute pancreatitis because they
have prognostic relevance and may precipitate
intervention by either interventional radiolo
gy or by the surgeons [26] (Fig. 7). Complica
tions of acute pancreatitis, such as abscess and
pseudoaneurysm formation, will be further
discussed in an upcoming issue of the AJR.
The imaging of acute pancreatitis using
MRI is comparable with that of CT, and the
same descriptive terminology is used [10, 28].
MRI may be performed using unenhanced and
contrast-enhanced T1-weighted and fat-sup
pressed T2-weighted gradient-echo sequences.
Typically, an enlarged edematous gland that is
low signal on T1-weighted and high signal on
T2-weighed MRI is observed [10]. Acute pan
creatitis is sometimes associated with pancreat
ic ductal dilatation, which can be clearly iden
tified and examined on T2-weighted images
[13] (Fig. 8). T2-weighted images are also use
ful for the detection of acute pancreatic collec
tions, pseudocysts, and hemorrhage [11]. The
pancreatic duct should be carefully reviewed
on T2-weighted images for the presence of dis
connection, which can be easily overlooked

[29]. Disconnection occurs when necrosis af

fects the ductal epithelium and an isolated seg
ment of viable pancreatic tissue is disconnect
ed from the duodenum. This creates persistent
fistulation and inflammation with an increased
incidence of infection [29]. Diagnosis of dis
connection of the main pancreatic duct requires
visualization of a necrotic region of at least 2
cm in size, viable pancreatic tissue proximal to
the necrosis, and extravasation at pancreatog
raphy [29]. The main pancreatic duct usual
ly enters the necrotic material at a 90 angle.
Evaluation for a disconnected pancreatic duct
may be performed with CT or MRI. Although
early MRCP is generally of limited value for
identifying the cause of acute pancreatitis be
cause collections may compress the pancreatic
and biliary ducts obscuring gallstones, MRCP
may be of benefit when iodinated contrast ad
ministration is contraindicated or if disconnec
tion of the main pancreatic duct is suspected
[29]. Secretin-enhanced MRCP may be used
for assessment of the pancreatic duct, although
concerns regarding the risk of increasing pan
creatic inflammation exist. Because ductal
pressures approaching those at ERCP cannot
be achieved, a normal MRCP is insufficient for
exclusion of a disconnected duct in the pres
ence of suspicious features [29].

W224

Conclusion
Imaging plays an important role in the
management of the patient with acute pan
creatitis. CT in particular has revolutionized
pancreatic imaging, and what was once con
sidered a hidden organ may now be accurate
ly and noninvasively imaged.
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Imaging of Acute Pancreatitis

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