Dr. Quencer, Dr. Kambadakone, Dr. Sahani, and Dr. Guimaraes are at the Division of Abdominal Imaging and Intervention, Massachusetts General Hospital, Boston, MA.
pancreas is a retroperitoneal organ situated deep within the abdomen
and not easily accessible by physical examination. Pancreatic
pathologies have a variety of presentations, which make their diagnosis
challenging to physicians.1 Imaging plays a critical role in
the evaluation of pancreatic diseases and provides valuable information
to clinicians, thereby dictating crucial management decisions.
Technological advancements in multidetector computed tomography (MDCT)
and magnetic resonance imaging (MRI), coupled with innovations in
3-dimensional(3D) imaging capabilities, have revolutionized the role of
imaging in managing patients with pancreatic disorders. Imaging is most
often performed to manage patients with pancreatitis and suspected
pancreatic mass lesions.
In Part 2 of this article, available on www.appliedradiology.com,
the discussion continues regarding imaging manifestations of various
abnormalities affecting the pancreas as they relate to specific types of
pancreatitis, pancreatic neoplasms, and tumors.
Normal anatomy and physiology
pancreas is a retroperitoneal organ located in the anterior pararenal
space posterior to the stomach and bounded by the c-loop of duodenum on
the right side. The pancreas is divided into the head, uncinate process,
neck, body, and tail. The head is situated within the duodenal c-loop,
while the tail lies in the splenic hilum slightly superior to the head.
Since the pancreas is unencapsulated, there is uninhibited spread of
tumor and inflammation to surrounding structures. The spleno-portal vein
confluence lies just posterior to the pancreatic neck and anterior to
the uncinate process. The splenic vein courses along the posterior
aspect of the pancreatic body and tail, while the celiac artery is
related cranially to the neck of the pancreas. The superior mesenteric
artery (SMA) arises from the aorta at the level of the pancreatic neck.
The head receives arterial blood supply from the common hepatic artery
via gastroduodenal artery (GDA) branches—the anterior andposterior
superior pancreatico-duodenal branches and the SMA-inferior
pancreatico-duodenal branches. These form an extensive arterial network
around the pancreatic head. The body and tail of the pancreas are
supplied by branches of the splenic artery, including the dorsal
The pancreas has two distinct
functions, endocrine and exocrine. Eighty to 95% of the pancreatic
parenchyma is composed of acinar cells, which are dedicated to the
exocrine functions of producing and secreting digestive enzymes, such as
trypsinogen, lipase. and amylase.3 It is curious to note
that while the overwhelming majority of the pancreatic parenchyma is
composed of acinar cells, acinar cell carcinoma is an extremely rare
subtype of pancreatic carcinoma (< 1% of all pancreatic tumors).4
Only 5% to 20% of the pancreatic parenchyma is responsible for the
endocrine function, composed of cells clustered into Islets of
Langerhans, which produce hormones, such as insulin, glucagon,and
Development and variants
the pancreas arises from a dorsal and ventral pancreatic bud. The
larger dorsal bud is the precursor of the anterior portion of head as
well as body and the tail, while the smaller ventral bud develops into
the posterior head and uncinate process. The dorsal and ventral ducts
fuse into one major duct, the duct of Wirsung, which empties into the
duodenum along with the common bile duct at the ampulla of Vater.1
Variations in the pancreatic ductal branching pattern are common
(Figure 1). One common variant is the presence of an accessory
pancreatic duct, known as the duct of Santorini, which empties into the
duodenum separately from the main pancreatic duct via the minor papilla,
which is superior to the ampulla. Another variant is the so-called
dorsal dominant drainage, where the duct of Wirsung empties into the
minor papilla and the duct of Santorini empties into the major papilla.
This is similar to pancreas divisum, which is present in about 10% of
normal individuals. However, in the pancreas divisum, there is complete
separation of the dorsal and ventral pancreatic ducts.5 An
association between the pancreas divisum and pancreatitis is described
and is believed to be due to the relative obstruction of the dorsal
pancreatic duct, which carries digestive enzymes from the majority of
the gland and empties through smaller minor papilla.6 This,
however, is controversial and other authors believe that pancreas
divisum is not causative in pancreatitis, but rather only associated
with other known genetic causes of acute and chronic pancreatitis, such
as CTFR, SPINK1, and PRSS1 associated mutations.7 Annular
pancreas can result during rotation of the ventral pancreatic bud as it
fuses with the dorsal bud, resulting in a ring of pancreatic tissue
encircling the duodenum, causing gastric outlet obstruction in infants
and pancreatitis in adults (Figure 2).
has a limited role in imaging of the pancreas, but it can sometimes
depict parenchymal calcifications, which helps in the detection of
chronic pancreatitis. However, punctate calcifications near the pancreas
can be confused with splenic artery calcifications. In patients with
pancreatitis, several plain radiographic features have been described,
including the so-called ‘colon cutoff sign,’ characterized by abrupt
termination of colonic gas shadow at the splenic flexure.
(US) also has a limited role in pancreatic evaluation as the overlying
gas from the transverse colon and stomach makes visualizing pancreatic
parenchyma difficult or even impossible. However, US can help identify
gallstones as an etiology in patients with pancreatitis and biliary
ductal dilation in patients with a pancreatic head mass. Most focal
pancreatic lesions are hypoechoic compared to normal parenchyma. The
advent of endoscopic US (EUS), has added a new dimension as it provides
ultra-high resolution images and exquisite details of pancreatic tumors,
particularly in cystic lesions. Additionally, EUS allows simultaneous
tissue sampling of pancreatic lesions withEUS-guided fine needle
aspiration (FNA). However, the acquisition and interpretation of these
images are usually performed by interventional gastroenterologists and
are not within the scope of this article.
MDCT is the modality of choice for the evaluation of both inflammatory and neoplastic conditions of the pancreas.2 In
inflammatory conditions, MDCT not only provides excellent visualization
of the parenchymal abnormalities, but clearly depicts the
extrapancreatic spread of disease. In pancreatic neoplasms, MDCT
accurately depicts the tumor morphology, ductal anatomy, and its
relationship to surrounding organs and vascular structures. Thin-section
MDCT in combination with image-processing techniques (multiplanar
reconstructions and curved reformations) can provide additional imaging
details and can define the pancreatic ductal anatomy.
specific MDCT imaging protocol depends on the clinical question to be
answered. A typical MDCT protocol for pancreatic evaluation involves
administration of oral and intravenous contrast (Table 1). For routine
indications, including pancreatitis, a portal venous-phase abdominal CT
with positive oral contrast medium (POCM) provides the most information.
However, for a dedicated pancreatic protocol CT, neutral oral contrast
media (NOCM) like water are preferred, as they allow superior image
reconstruction.8 In patients with suspected pancreatic mass,a
focused pancreatic protocol CT is performed, which includes a
pancreatic, portal venous, and a delayed phase through the liver to
assess for hepatic metastases. An arterial phase may be performed in
place of a pancreatic phase if a hypervascular pancreatic lesion like a
neuroendocrine tumor is suspected. Pancreatic phase refers to the late
arterial phase (typically 40-45 sec after contrast injection) during
which there is maximal differentiation between the normal parenchyma and
hypodense pancreatic tumors like adenocarcinoma. This phase also
provides optimal arterial and mesenteric venous opacification, which
allows assessment of vascular involvement, thereby permitting surgical
planning by evaluating potential tumor resectability. Arterial
opacification in this phase limits the need for a separate dedicated
arterial phase. Accurate contrast timing for image acquisition during
various phases can be achieved using the test bolus or the automatic
bolus triggering technique.
resonance imaging (MRI) with cholangiopancreatography (MRCP) has emerged
as a reliable tool for accurately characterizing pancreatic
pathologies. The superior soft-tissue and contrast resolution inherent
to MRI makes it a superior test for assessing the morphologic features
of pancreatic tumors particularly in pancreatic cysts. MRCP provides
excellent 2-dimensional (2D) and 3-dimensional (3D) depiction of the
pancreatic duct anatomy and its abnormalities in patients with
pancreatitis as well as neoplasms.
imaging sequences used include axial T1-weighted images, with and
without fat saturation, using breath-hold or gated respirations. A
complete evaluation of the pancreatic parenchyma and pancreatico-biliary
ductal system can be performed with the following sequences:
T1-weighted gradient echo, T2-weighted (T2W) axial, and coronal
sequences, either fast spin echo (FSE) or turbo spin echo(TSE), 2D and
3D MRCP; and T1-weighted 3D gradient-echo before and after gadolinium.
To adequately visualize the gallbladder and to assess the exocrine
response to secretin, the patient should ideally be fasting for 4 hours.
Negative oral contrast is administered to reduce the signal from the
overlying stomach and duodenum. Axial and coronal T2 images with and
without fat saturation should also be obtained.Dynamic postcontrast
images should be obtained 25, 70, and 120 sec after the gadolinium
contrast injection. Ideally, field strength should be≥ 1.0 Tesla with
fast imaging sequences. A standard pancreatic protocol also includes
MRCP images for further evaluation of pancreatic ductal abnormalities.
The MRCP sequence can be obtained as 2-dimensional (2D) or a
3-dimensional (3D) acquisition. 3D MRCP produces high resolution images
of the pancreato-biliary ductal anatomy as the thin sections without
slice gap of a 3D technique allows better assessment of small stones,
side branches of the main pancreatic duct, and intrahepatic bile ducts.
The 2D MRCP is acquired either as a thick-slab, single-shot,fast spin
echo T2W sequence or a multisection, thin-slab, single shot FSE T2W
sequence. The 3D fast spin echo sequence can either be acquired as a
series of breath holds or during free breathing. Secretin MRCP is a
modified MRCP sequence, which entails administration of secretin to
stimulate the exocrine function of the pancreas. Secretin MRCP is useful
in assessment of complex ductal anomalies and to quantitatively or
semiquantitatively assess the exocrine function of the pancreas.
US, the pancreas is slightly echogenic compared to the liver and has a
homogenous appearance. On MDCT, the normal pancreas has slightly higher
attenuation than the paraspinal muscles and has a lobulated contour. On
contrast administration, it enhances fairly homogenously (up to 100-150
HU) with slight attenuation differences (< 30 HU) between the head
and tail, which can be a normal variant.9 Fatty infiltration
of the pancreas can occur with normal aging, but is also seen in
pathologic conditions, such as obesity, cystic fibrosis, and rarer
conditions, such as Schwachman-Diamond syndrome and Johnson-Blizzard
syndrome (Figure 3).2
The normal pancreas has the
highest intrinsic T1 signal of all abdominal organs and therefore
precontrast T1-weighted images are the most sensitive sequence to detect
focal lesions, which are often hypointense relative to normal
parenchyma and for detection of hemorrhage within inflammatory
collections. On T2-weighted images, the pancreas is slightly
hyperintense compared to the adjacent muscle, and they are optimally
suited for depicting the ductal anatomy, cystic lesions, and islet cell
tumors, which are hyperintense compared to normal pancreas.5
pancreatitis refers to acute reversible inflammation of pancreatic
parenchyma. Approximately 200,000 patients with this condition are
admitted to the hospital each year in the United States (U.S.).10
It is triggered by premature activation of digestive enzymes within the
pancreatic parenchyma, leading to digestion of pancreatic
andperipancreatic tissues. The etiology for acute pancreatitis includes
gallstones (40%), alcohol abuse (30%-35%), andidiopathic causes (20%).
Other etiologies include mechanical (post ERCP, trauma), metabolic
(hypercalcemia, hypertriglyceridemia, cystic fibrosis, and hereditary
pancreatitis) and toxic (drugs like HCTZ and aspariginase).1
The overall mortality rate for pancreatitis is 2% to10%, but most
(70%-80%) patients experience mild or edematous pancreatitis, which is
typically a self-limiting disease with a mortality of< 1%. On the
other hand, approximately 25% of patients experience severe
pancreatitis, which is associated with high morbidity and a mortality
rate between 10% and 23%. The dichotomy between these two outcomes is
highly correlated with the presence or absence of pancreatic necrosis,
which is seen in nearly 20% of all cases.11 Pancreatic
necrosis is caused by disruption of the microcirculation via necrotizing
vasculitis and thrombosis and is an important prognostic indicator.
Mortality rises with the degree of pancreatic necrosis and mortality
rates of > 50% are seen when necrosis involves > 30% of pancreatic
parenchyma.12 The necrotic tissue can get secondarily infected due to translocation of gut flora and is nearly always fatal if untreated.13 The treatment typically entails surgical debridement or percutaneous drainage.
Imaging in acute pancreatitis
The diagnosis of acute
pancreatitis is often based on clinical and laboratory evidence. Imaging
is therefore performed in patients with pancreatitis not for diagnosis
but for the following reasons: (i) to identify the possible etiology
(such as gallstones or neoplasm), (ii) to grade the severity, (iii) to
evaluate complications, and (iv) to identify possible distinctive
imaging features in special types of pancreatitis, such as tropical
pancreatitis, autoimmune pancreatitis, or groove pancreatitis.2,9
Additionally, CT has been shown to be a better predictor of
complications, mortality, and length of hospital stay than either the
Ranson or APACHE II criteria.14
MDCT is the preferred
imaging modality and contrast administration is essential to detect
complications, such as parenchymal necrosis, venous thrombosis, and
arterial pseudo-aneurysm. A single portal venous phase abdominal MDCT is
performed for routine cases,but arterial phase scanning is imperative
when pseudoaneurym is suspected. The range of pancreatic findings and
the CT grading is depicted in Table 2. Mild or early pancreatitis (Grade
A) is occult on CT and the imaging findings lag behind the clinical and
laboratory findings. Grade B pancreatitis is characterized by diffuse
or focal pancreatic enlargement, while peripancreatic inflammatory
changes,including blurring of the pancreatic margin, stranding of
adjacent fat, and mild decrease in parenchymal density from edema occur
inGrade C pancreatitis (Figure 4). Thickening of the anterior renal
fascia (Gerota’s fascia) is also seen and is an early and sensitive
indicator of peripancreatic inflammation. MRI is typically performed for
evaluation of etiologies, such as gallstones or pancreas divisum. The
imaging findings include loss of normal T1 hyperintensity with
heterogeneous hypointense areas. T2 fat-suppressed images may show small
amounts of peripancreatic fluid.
detecting pancreatic necrosis is of paramount importance in imaging
pancreatitis. On both MDCT and MRI, pancreatic necrosis appears as
diffuse or focal parenchymal areas without enhancement (Figure 5).
Additionally, MRI depicts areas of hemorrhage within necrotic foci as
ill-defined areas of high T1 and low T2 signal. On MDCT, false positive
diagnosis can result from areas of decreased attenuation due to focal
fatty replacement, edema, or intrapancreatic fluid collections. False
negative scans occasionally occur when imaging is performed early in the
phase of pancreatic inflammation (first 12-24 hours after symptom
onset). Although necrosis occurs early, the false negative rate can be
reduced if CT is performed 72 hours after symptom onset. Overall, MDCT
has been reported to have 87% accuracy and 100% specificity in the
detection of necrosis involving > 30% of the gland.9
fluid collections often occur in patients with pancreatitis, and the
presence of fluid collections increases the CT pancreatitis grade.
Pseudocysts are the most common inflammatory cystic pancreatic lesions
and contain necrotic debris from digested retroperitoneal fat. While
their definitive diagnosis requires aspiration of contents to show a
high amylase level, a preceding history of pancreatitis with the typical
imaging features, such a fluid collection with a distinct fibrous
capsule persisting for > 4 weeks allows for a confident presumptive
diagnosis. Pseudocysts can have myriad imaging appearances ranging from
unilocular to multilocular morphology. Enhancement of the cyst wall is
commonly seen on MDCT. On MRI, they typically show variable but low
signal on T1-weighted images and high signal on T2-weighted images.
Hemorrhage and debris can cause an atypical appearance leading to an
increased T1 signal and decreased T2 signal compared to simple appearing
pseudocysts. Many pseudocysts demonstrate communication with the main
pancreatic duct, best seen with either ERCP or MRCP.2
Pseudocysts are typically treated conservatively unless complications,
such as mass effect, infection, and rupture leading to peritonitis,
arise (Figures 6 and 7). Gas within a pseudocyst does not prove
infection; this imaging finding could also be due to enteric fistula or
recent intervention. Percutaneous, endoscopic or open surgical drainage
are treatment options.
of the digestive pancreatic enzymes can cause digestion of the wall of
the surrounding arteries leading to weakening and pseudoaneurysm
formation (Figure 8). The splenic artery is most commonly involved,
followed by the gastro-duodenal artery, celiac artery, orSMA. They are
at a high risk for hemorrhage and urgent surgical or vascular
interventional radiology evaluation is needed. Pancreatic and
peripancreatic inflammation can extend to surrounding venous structures
leading to thrombosis, which manifests as a filling defect within the
affected vessel during the portal venous phase.
traditionally chronic pancreatitis has been thought of as a separate
entity from acute pancreatitis, given that recurrent episodes of acute
pancreatitis occasionally lead to chronic pancreatitis, acute and
chronic pancreatitis are now thought be on a spectrum of a similar
Chronic pancreatitis, which results in
irreversible fibrosis, atrophy, and exocrine and endocrine insufficiency
of the pancreas, may manifest clinically as malabsorption and diabetes.
MDCT is the preferred
modality to image chronic pancreatitis owing to better visualization of
calcifications (Figure 9). Pancreatic calcifications may be parenchymal
or ductal in origin. The gland may become focally or diffusely atrophic.
Pancreatic ductal dilatation with a beaded appearance is a
characteristic appearance in chronic pancreatitis. Occasionally, chronic
pancreatitis may result in an inflammatory pseudomass causing focal
enlargement with fibrosis and hypoenhancement and inflammatory narrowing
of the common bile duct, which can mimic adenocarcinoma. The presence
of calcifications and smooth tapered narrowing of the CBD allow
differentiation of inflammatory pseudo mass from adenocarcinoma, which
results in abrupt narrowing of the common bile duct.2 The MRI
findings are similar to MDCT appearance. However, pancreatic
calcifications are not well seen on MRI. Inflammatory pseudo mass has a
decreased signal intensity on T1-weighted images secondary to fibrosis
and decreased protein content of the gland from atrophy. Dilatation of
pancreatic side branches is more apparent on MRI than CT and may cause
the so called “string of pearls” or “chain of lakes” appearance on MRCP.5
Part 2 of this article is available at www.appliedradiology.com.
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- Shanbhogue A, Fasih N, Surabhi V, et al. A Clinical and radiologic review of uncommon types and causes of pancreatitis. Radiographics. 2009;29: 1003-1026.
- Pezzilli R. Pancreas divisum and acute or chronic pancreatitis. JPancreas. 2012;13:118-119.
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Singla A, Csikesz N, Simons J, et al. National hospital volume in acute
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- Baron TH, Morgan DE. Acute necrotizing pancreatitis. N Engl J Med. 1999;340:1412-1417.
- Balthazar EJ, Robinson DL, Megibow AJ, Ransson JH. Acute pancreatitis: Value of CT in establishing prognosis. Radiology. 1990;174:331-336.
- Banks PA. Infected necrosis: Morbidity and therapeutic consequences. Hepatogastoenterology. 1991;38:116-119.
Leung TK, Lee CM, Lin SY, et al. Computed tomography severity index is
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- Braganza J, Lee S, McCloy R, McMahon M. Chronic pancreatitis. Lancet. 2011;377:1184-1197.