Imaging in Chronic Pancreatitis - State of The Art Review

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Hepatobiliary and Pancreatic Imaging

Imaging in chronic pancreatitis: State of


the art review
Rohan Kamat, Pankaj Gupta1, Surinder Rana1
Department of Radiodiagnosis and Imaging and 1Gastroenterology, PGIMER, Chandigarh, India

Correspondence: Dr. Pankaj Gupta, Department of Gastroenterology, Section of Radiology, PGIMER, Chandigarh, India.
E‑mail: [email protected]

Abstract
Chronic pancreatitis (CP) is an important gastrointestinal cause of morbidity worldwide. It can severely impair the quality of life
besides life‑threatening acute and long‑term complications. Pain and pancreatic exocrine insufficiency (leading to malnutrition)
impact the quality of life. Acute complications include pseudocysts, pancreatic ascites, and vascular complications. Long‑term
complications are diabetes mellitus and pancreatic cancer. Early diagnosis of CP is crucial to alter the natural course of the disease.
However, majority of the cases are diagnosed in the advanced stage. The role of various imaging techniques in the diagnosis of
CP is discussed in this review.

Key words: Chronic pancreatitis; diagnosis; imaging

Introduction steatorhea and diabetes.[2] Early diagnosis of CP is difficult.


Biochemical studies do not help in definitive diagnosis in the
Clinically, morphologically, and histologically, pancreatitis early stages.[6] Diagnosis at this stage is suspected based on a
can be categorized into acute and chronic. [1] Chronic combination of clinical symptoms, pancreatic function tests,
pancreatitis (CP) is characterized by relentless inflammatory and radiological investigations.[7] Definitive diagnosis of CP
and fibrotic changes of the gland, eventually leading is established in advanced cases with a destruction of greater
to exocrine and endocrine dysfunction. [2] CP due to than 90% of parenchyma.[8] Several imaging modalities
alcoholism constitutes about 70-90% of cases in western have been used to assess the pancreas such as abdominal
countries. Malnutrition is a rare cause of CP now.[3,4] Other radiographs, ultrasonography, computed tomography (CT),
important risk factors are genetic predisposition, smoking, magnetic resonance imaging  (MRI), and endoscopic
high protein diet, hypercalcemia, hyperparathyroidism, retrograde cholangiopancreatography (ERCP).[2] With the
congenital lesions like abnormal pancreaticobiliary junction evolution of several newer techniques such as pancreatic
and pancreatic divisum, pancreatic or periampullary CT protocol with a multi‑detector scanner, magnetic
neoplasms, and ampullary stricture. Rarer causes of CP resonance cholangiopancreatography (MRCP) with secretin
include hereditary pancreatitis, autoimmune pancreatitis, stimulation  (S‑MRCP), endoscopic ultrasound  (EUS)
and chronic renal failure.[2] Gall stones are major causes of and shear wave elastography (SWE), early detection and
acute pancreatitis. However, they are not considered as management of CP has been possible.[8] In the early phases
risk factors for chronic pancreatitis.[5] CP most commonly of CP, functional and morphological disturbances can be
presents with abdominal pain. It can also present with seen at the ductal level, with delayed discharge of pancreatic

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DOI:
10.4103/ijri.IJRI_484_18
Cite this article as: Kamat R, Gupta P, Rana S. Imaging in chronic pancreatitis:
State of the art review. Indian J Radiol Imaging 2019;29:201-10.

© 2019 Indian Journal of Radiology and Imaging | Published by Wolters Kluwer ‑ Medknow 201


Kamat, et al.: Imaging in chronic pancreatitis

enzymes in response to secretin (functional) or ectasia and


irregularities of the main/branch ducts (morphological).[2,9]
Chronic inflammation of the pancreas results in fibrosis of
the gland with loss of exocrine tissue. Edema, inflammation,
and necrosis may superimpose on this background.
Pancreatic biopsy is not usually performed as it may result
in several complications such as acute pancreatitis, fistulae,
and hemorrhage. It may also yield false negative results due
to sampling of normal pancreatic tissue.[5] In this review, we
will discuss the role of various imaging modalities in CP.

Pancreatic functional tests


Functional assessment of the pancreas can be carried out
directly by assessing the volume of secretions, bicarbonate,
and measuring the enzyme levels in blood and stools.
Pancreatic enzymes play a key role in digestion. Hence,
indirect evaluation involves studies on mal‑digestion to
prove pancreatic insufficiency.[10,11]

Overall, noninvasive tests are useful only in moderate to


severe pancreatic insufficiency.[12] None of these tests are
useful in mild stage of the disease. Mixed triglyceride Figure 1: Plain abdominal radiograph shows extensive pancreatic
breath test is one such test which has shown a promising calcifications (arrows)
role in monitoring of the patients on enzyme replacement.[10]
But like other breath tests, it is not useful in identifying with fluids or scanning the patient in oblique position using
the disease at an early stage. Secretin-cholecystokinin spleen as the acoustic window. This technique especially helps
and endoscopy‑based functional testing are useful in the in visualization of the tail of the pancreas. Other techniques
diagnosis of CP when morphological assessment cannot are asking the patient to bloat the abdomen during the scan
yield the diagnosis in early stages of the disease. These and scanning in sitting position. However, as ultrasound is
tests however are invasive, expensive, time consuming, easily available, cheap, and has no risk of ionizing radiation,
nonstandardized, and are available only in a few centres. it is used as the first line tool in the radiological assessment
They are also not suitable for monitoring the patients on of pancreas. [2,6,10] Pancreas is usually iso/hyperechoic
replacement therapy. Hence, they are not widely being compared with normal hepatic parenchyma. In early stages
used.[10,13] Recent improvements in MRI such as S‑MRCP of CP, ultrasound is seldom useful.[4,5] In later stages of the
have helped in morphological evaluation of the pancreatic disease, there are focal hypoechoic areas and hyperechoic
duct along with the assessment of pancreatic secretions.[13] areas within the gland representing inflammatory and
fibrotic tissues, respectively. Hence, CP gives a heterogenous
Imaging modalities appearance to the pancreas. Pancreatic parenchyma shows
Radiographs: Radiograph is now an obsolete tool for the progressive atrophy in CP. Irregular progressive dilatation
diagnosis of CP. The utility of radiographs in CP is restricted of the main and the branch pancreatic ducts is seen over
to detection of focal calcifications along the course of time. Discontinuous strictures within the duct may give a
pancreas, in the epigastric region [Figure 1]. Calcifications in “chain of lakes” appearance. Punctate calcifications with
CP is the most specific feature, however, it occurs late in the or without posterior acoustic shadowing, in the pancreatic
course of the disease. Radiographs have a poor sensitivity parenchyma and the ducts, is the hallmark of CP, seen in
in the diagnosis of CP.[2] about 40% cases [Figure 2].[5,14‑16] Tiny calcifications not seen
on routine sonogram can be identified with color Doppler as
Ultrasonography: Pancreas is a retroperitoneal organ. a result of twinkling artifacts.[14] Associated pancreatic ductal
Ultrasonography of pancreas is challenging due to the calculi may be seen which might obstruct the ducts resulting
bowel gas shadows obscuring part or whole of the pancreas. in repeated attacks of pancreatitis. Other important findings
Sonography of pancreas is also dependent on the patient’s in CP that can be detected with sonography are pseudocysts,
body habitus and the radiologist’s skill. Pancreas should thrombosis of the splenoportal axis, and portosystemic
always be assessed in fasting status as this can restrict the collaterals and arterial complications like aneurysms most
obscuration of the gland by bowel gases. Graded compression commonly of splenic artery or gastroduodenal artery.[17]
can help to displace the bowel gases and result in better
visualization of the pancreas. Several manoeuvres have been Endoscopic Ultrasonography (EUS): Transabdominal
used to assess the pancreas such as distending the stomach sonography has a limited scope in the assessment of
202 Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019
Kamat, et al.: Imaging in chronic pancreatitis

A B
Figure 3 (A and B): EUS in a patient with chronic pancreatitis shows
echogenic strands (arrow) in the head of pancreas (A). EUS in another
patient with chronic pancreatitis (B) shows dilatation of main pancreatic
duct (arrow) and side branches (short arrow)

Rosemont criteria for EUS diagnosis of CP is shown in


Table 1.[24]
Figure 2: Abdominal ultrasound shows atrophic pancreas with dilated
main pancreatic duct (short arrow) with intraductal calculi (arrow) Contrast enhanced‑EUS (CE‑EUS) is an emerging
technique in imaging the pancreas. It is particularly useful
pancreas in obese individuals and gaseous abdomen. in patients with renal failure as the microbubble contrast
This limitation is overcome by EUS, as the high frequency agents are not nephrotoxic. The contrast resolution of
transducer (5-12.5 MHz) in EUS is in close proximity to the EUS is further improved with the use of these contrast
pancreas, hence visualizing it better.[10,14] EUS like ERCP and
agents.[25] The lobular pattern seen in the conventional EUS is
S‑MRCP helps in diagnosing CP at early stages. Normal
exaggerated by CE‑EUS. CP patients have a faster wash‑out
pancreas in EUS shows homogenous appearance, smooth
of the contrast compared with normal individuals.[26]
margins, and is slightly hyperechoic to liver (salt pepper
Pancreatic carcinoma appears as a hypoenhancing lesion
appearance). Normal main pancreatic duct is tubular with
in CE‑EUS showing rapid wash out. Mass forming CP
anechoic walls. Normal side branches can be seen in about
usually appears as an isoenhancing lesion. Hypoenhancing
32% patients.[15,16] Certain features of CP seen in EUS besides
character of the adenocarcinoma has a high sensitivity
the usual features seen in TAS and CT are subtle lobularity
of 89-96%, but advanced mass forming CP can give a
of the gland borders, tiny cystic changes within the
similar appearance [Figure 4]. Hyperenhancement of the
glandular parenchyma, echogenic foci/strands representing
lesion however rules out an adenocarcinoma.[27] EUS and
areas of fibrosis [Figure  3A], side branch ectasia, and
MRI/S‑MRCP have similar sensitivities for the diagnosis
echogenic margins of main pancreatic duct [Figure  3B].
EUS due to its superior resolution compared with TAS and of CP. EUS has a slightly greater specificity. Combining
CT helps in early diagnosis of CP by detecting the subtle both EUS and MRI/S‑MRCP, the specificity was found to
parenchymal and ductal changes.[5] Differentiation of mass be 100%.[28]
forming pancreatitis is difficult with EUS per se, like other
modalities. However, EUS has the ability to sample the EUS-secretin pancreatic function test (EUS-PFT):
tissue by guided fine needle aspiration (EUS‑FNA).[4,5,18‑20] In Demonstration of exocrine insufficiency is a functional
a retrospective analysis by Agarwal et al., it was found that evidence of CP, which may be present in a mild form even
EUS‑FNA had a sensitivity of 88.8% and specificity of 100% at the onset of pancreatic fibrosis. The gold standard for
for diagnosis of mass forming pancreatitis.[21] In comparison diagnosis of early exocrine insufficiency in CP is direct PFT
with ERCP, EUS is relatively less invasive, assesses both using secretin and CCK. EUS-PFT allows a simultaneous
parenchymal and ductal abnormalities, can be used for structural and functional assessment of the pancreas.
celiac plexus blockade, and drainage of collections.[18] It has Following intravenous administration of synthetic secretin,
a sensitivity and specificity of 83% and 80%, respectively, duodenal aspirates are collected at 15, 30, and 45  min.
for the diagnosis of CP.[22] Drawbacks of EUS are its inter/ A  peak bicarbonate concentration less than 80 mM is
intraobserver variability and false positivity, as a few suggestive of exocrine insufficiency.
findings of CP like echogenic septations can be normally
seen with aging, in smokers and in alcoholics.[5] A few Elastography: Elastography is a noninvasive ultrasound
studies have shown that EUS is more sensitive than ERCP.[23] technique which helps to assess the stiffness of a tissue.
Kahl et al. conducted a study comparing ERCP with EUS and Elastography can be qualitative or quantitative. The stiffness
found that 69% of patients detected by EUS and negative of the region of interest  (ROI) can be quantified either by
on ERCP in the initial study eventually showed abnormal conventional strain elastography  (SE) or by shear wave
pancreatograms.[23] elastography  (SWE). Fibrosis and malignant infiltration

Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019 203
Kamat, et al.: Imaging in chronic pancreatitis

Table 1: Rosemont criteria for EUS diagnosis of CP[24]


Major Criteria Minor criteria
Major A Cysts
Hyperechoic foci with shadowing MPD calibre ≥3.5 mm
MPD calculi Irregular ductal contour
Major B Side branch ectasia ≥1 mm
Lobularity with honeycombing Echogenic duct walls and strands
Non‑shadowing hyperechoic foci
Lobularity with non‑contiguous lobules
I. Consistent with CP II. Suggestive of CP III. Indeterminatefor CP IV. Normal
A. 1 major A feature (+) ≥3 minor features A. 1 major A feature (+) < 3 minor features A. 3 to 4 minor features, no major features ≤2 minor
B. 1 major A feature (+) major B feature B. 1 major B feature (+) ≥3 minor features B. major B feature alone or with <3 minor features and no
C. 2 major A features C. ≥5 minor features (any) features major features

A B C
Figure 4 (A-C): Contrast‑EUS in a patient with mass forming
chronic pancreatitis shows a mass in the head of pancreas with
cystic component (arrow, A) with peripheral enhancement (arrow, B) A B
and central nonenhancing component. The central nonenhancing
Figure 5 (A and B): EUS elastography in a patient with chronic
component is slightly echogenic than the rest of the mass (arrow, C).
pancreatitis shows heterogenous stiffness of the pancreas (A) with
In long standing cases of mass forming chronic pancreatitis, this lack
hard areas (arrow) and areas of intermediate stiffness (short arrow). In
of enhancement mimics pancreatic adenocarcinoma
another patient with mass forming chronic pancreatitis (B), elastography
shows that the mass is hard (blue areas). Also note the presence of
can cause increase in the hardness of a tissue. As the first a cyst (arrow)
generation strain elastography was qualitative, second
generation systems were developed, which gave the strain Table 2 shows the SR of Rosemont categories.
ratio  (SR). ROIs are drawn over the target region and the
surrounding reference region  (preferably in the gut wall). As discussed above, CE‑EUS, EUS elastography, and EUS
Then the SR is calculated.[21,22,25] SWE quantitatively determines FNA are the newer modalities which have improved the
the stiffness of the tissue based on the velocity of shear waves confidence in differentiating a focal pancreatic mass in CP
in the tissues. Both SWE and SE yield elastograms, which from a malignant tumor.[26]
are color maps superimposed on the gray‑scale images. The
color pattern determines the degree of stiffness (blue being Computed tomography
towards the hard end of the spectrum and red towards the CT features of CP are shown in Table 3.[35‑38]
soft end).[29] Elastography can be used with TAS or EUS.[30]
In CP, fibrosis of the gland leads to progressive increase in Calcifications are seen in the late stages of CP and hence
glandular stiffness [Figure 5A].[31] Focal pancreatic lesions can detection of CP in early stages using CT is difficult
also be evaluated with EUS elastography to determine the [Figure 6A]. Sensitivity of CT in detecting late stages of CP
nature based on the strain pattern.[32] EUS shows both focal is 60-95%.[8] Alcohol‑induced pancreatitis and hereditary
pancreatic masses in CP as well as in adenocarcinomas as pancreatitis show calcifications in the gland at a relatively
hypoechoic masses. Inflammatory masses of pancreas can earlier stage than in other causes of pancreatitis like
show varied range of strain ratios [Figure  5B], however a obstructive CP and cystic fibrosis‑related CP.[39] Presence
hypoechoic lesion with higher strain suggesting softer tissue and number of parenchymal calcifications is an independent
is unlikely to be malignant.[14] predictor of the degree of pancreatic fibrosis.[40] Multiphase
protocol is now commonly used in the assessment of
SR also helps in predicting the exocrine insufficiency pancreas, which includes a precontrast scan which helps
of pancreas. [33] With progression of disease, there is in excellent depiction of calcifications, a pancreatic phase
corresponding decline in the exocrine activity of the which is the best phase to assess the arterial enhancement
gland. EUS elastography helps in predicting the enzymatic for surgical mapping and to study the arterial complications,
deficiency, suggesting requirement of enzyme replacement followed by a venous phase which shows enhancement of
therapy in CP.[34] the pancreatic parenchyma. This phase is best suited to
204 Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019
Kamat, et al.: Imaging in chronic pancreatitis

A B C

A B

D E F
Figure 6 (A-F): CT findings in chronic pancreatitis: Non‑contrast
CT (A) shows extensive pancreatic calcifications (arrows). CT scan in
another patient (B) shows pancreatic atrophy (arrow) and a small cystic
area (short arrow). Pancreatic duct irregularity and varying degrees of
dilatation is shown in C to E (arrow). A large pseudocyst is also seen
in d. An intraductal calculus (arrow) with pancreatic head mass is seen C D E
in another patient (F) Figure 7 (A-E): Diffusion weighted MRI (DWI) in normal patient and
patient with chronic pancreatitis: Axial T1‑weighted image  (A) in a
evaluate the parenchyma, pancreatic duct, focal lesions, normal subject shows diffuse hyperintensity of the pancreas (arrow).
and collections [Figure 6B]. The corresponding DWI (B) shows no diffusion restriction (arrow). Axial
T1‑weighted image in a patient with focal autoimmune pancreatitis (C)
shows a hypointense lesion in tail of pancreas. On corresponding
Dilatation of the duct and parenchymal atrophy are less DWI (D) and ADC (E), there is evidence of diffusion restriction (arrow)
specific features than calcifications, as they can be seen in
normal aging as well.[4] The dilated duct could be smooth, Table 2: SR of Rosemont categories[33]
irregular, or beaded [Figure 6C-E].[3] The main pancreatic Normal pancreas 1.80 (95% CI: 1.73-1.80) P<0.001
duct may show intermittent areas of strictures and dilatation Indeterminate of CP 2.40 (95% CI: 2.21-2.56)
with pleomorphic ductal calculi [Figure 6F].[2] The calculi in Suggestive of CP 2.85 (95% CI: 2.69-3.02)
hereditary pancreatitis, tropical pancreatitis, and in genetic Consistent with CP 3.62 (95%CI: 3.24-3.99)
mutation‑related CP other than in cystic fibrosis are usually
large (2-5 cm), in comparison to the ones in alcohol‑related
Table 3: CT Features of CP
CP.[2,41,42] MRI/MRCP has superseded CT in detection of
Common findings % of cases
pancreatic ductal abnormalities, however CT is still the
Ductal dilatation 68%
preferred modality to assess the complications of CP.[43]
Parenchymal atrophy 54%
Magnetic Resonance Imaging (MRI) Parenchymal/ductal calcifications most specific feature[2] [Figure 4] 50%
MRI/MRCP features of CP are shown in Table 4. [44‑51] Collections 30%
Glandular enlargement due to interlobular and periductal fibrosis[17,35] 30%
Normal pancreas appears diffusely hyperintense on Bile duct dilatation 29%
T1‑weighted images due to the presence of proteinaceous Peripancreatic fat stranding 16%
enzymes [Figure  7A]. Fat saturated sequence helps in Less common findings
suppressing the retroperitoneal fat and thus improves Heterogenous glandular enhancement (Delayed enhancement of the fibrosed
parenchyma)[35]
the contrast between the hyperintense pancreas and the
Diagnosis of obstructive causes of CP such as pancreatic ductal carcinomas,
fat‑suppressed retroperitoneum.[8] Recently, diffusion cystic tumours and rarely neuro‑endocrine tumours which may lead to
imaging has evolved in the assessment of pancreatic recurrent episodes of pancreatitis.
diseases. Normal pancreas shows no restriction of Complications of CP:[35,36]
diffusion due to presence of free movement of the water Pseudoaneurysms
Biliary obstruction
molecules [Figure  7B]. Hence, the apparent diffusion Venous thrombosis
coefficient (ADC) is high in normal pancreas. In cases of CP, Rare complications such as pancreatic‑pleural and peritoneal fistulae can also
there is restriction of diffusion of water molecules resulting be suspected on CT due to presence of pleural fluid and ascites respectively,
in a drop in ADC [Figure 7C-E].[45,52] The limitations with however MRI/MRCP is superior in identifying these fistulae[37]
MRI assessment of abdomen due to respiratory motions,
peristalsis, and cardiac pulsations have been tackled Addition of MRCP sequence to the routine pancreatic MRI
effectively with the help of improved MRI techniques. has significantly improved the ductal assessment [Figure 8].
Faster acquisition and improved signal‑to‑noise ratio has As MRCP is a noninvasive tool, it has preferred over ERCP
been achieved with the current techniques.[50] for the diagnostic imaging of bile duct and pancreatic ducts.

Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019 205
Kamat, et al.: Imaging in chronic pancreatitis

S‑MRCP second parts of the duodenum while grade 3 is fluid


A s M R I / M R C P f a i l s t o e va l u a t e t h e e x o c r i n e filling the third part of the duodenum as well.
insufficiency, Matos et al. proposed a technique called
secretin‑stimulated MRCP  (S‑MRCP). [53] Secretin is a Grade 1 and 2 suggest exocrine insufficiency. This
polypeptide amino‑acid which is normally secreted quantification also correlates well with the fecal elastase
by the S cells of the duodenal mucosa. This enzyme is 1 value. [54] Thus S‑MRCP helps in morphological and
responsible for the bicarbonate‑rich secretions from the functional assessment of the pancreas.[54] Studies have also
pancreas, into the duodenum.[51] Prior to the procedure, evaluated the pancreatic exocrine function using diffusion
the patient should be fasting for 4-6 h. Half hour prior weighted imaging with S‑MRCP. As secretin injection
to the study, a negative oral agent is administered to increases the exocrine secretion and promotes diffusion of
suppress the signals from the pre‑existing bowel fluids. water, ADC is expected to rise in normal pancreas. However
Pre‑secretin images are first obtained. Secretin is injected in cases of CP, there is delay in the peak of ADC beyond
intravenously following which a series of T2‑weighted 10 min of secretin injection. Hence, ADC peak time after
images are acquired every 30 s for 15  min. Normal secretin stimulus can be used as a marker for pancreatic
main pancreatic duct shows dilatation which reaches a exocrine insufficiency in cases of CP.[56‑58]
peak in about 2-5 min.[54] Post‑secretin dilatation of the
main pancreatic duct should be at least 1 mm greater ERCP which was once considered as the gold standard test
than the baseline images to suggest ductal compliance. for CP is seldom used for diagnosis of CP at present. MRCP
Conventional MRCP fails to demonstrate the side is now preferred for diagnosis of CP. Agreement of 83–100%
branches. However, S‑MRCP shows the dilated side for ductal dilatation [Figure 9A], 70–92% for identification
branches in cases of CP.[55] Depending upon the volume of strictures [Figure 9B], and 92–100% for identification of
of fluid secreted into the duodenum, the exocrine function filling defects [Figure 9C] has been revealed on comparison
is assessed by three grades. Grade 1 is fluid restricted to of MRCP and ERCP.[59]
the duodenal bulb. Grade 2 is fluid filling the first and
18-F-flouro-deoxy-glucose positron emission tomography
(FDG PET): In order to obtain both biochemical and

A B C

A B Figure 9 (A-C): MRCP findings in chronic pancreatitis: Multiple


Figure 8 (A and B): MRI findings in chronic pancreatitis: Axial strictures (arrow) as well as filling defects (short arrow) within the main
T1‑weighted contrast enhanced MRI (A) shows reduced T1‑weighted pancreatic duct are seen in A. In another patient (B), a large intraductal
signal of the pancreas (arrow). Axial T1‑weighted contrast enhanced calculus  (arrow) is causing marked dilatation of the pancreatic
MRI in another patient (B) shows mild reduction in bulk with a cystic duct. MRCP in a different patient (C) shows strictures  (arrow) and
lesion in neck of pancreas (arrow) irregularity (short arrow) of the pancreatic duct

Table 4: MRI/MRCP Features of CP


MRI protocol: T1‑w FSE, T2‑w FSE, Pre/Post gadolinium GRE, MRCP[17]
T1: Hypointense areas corresponding to the inflammation/fibrosis/focal lesion[44‑46] [Figure 7B]
Contrast enhanced T1: Heterogenous signals and delayed post‑gadolinium enhancement due to presence of fibrotic areas which impede the capillary flow[8,47‑49]
Reduced antero‑posterior thickness of the pancreas [Figure 8]
Calcifications and ductal calculi show signal drop (Calcifications and air specks are better appreciated on CT)
MRCP: Most useful for ductal assessment [Figure 9A to C]
S‑MRCP: Assessment of pancreatic secretory functions
Modified MRCP Cambridge criteria for CP[51]:
Cambridge 1 (normal) Normal pancreas
Cambridge 2 (equivocal) Dilatation/obstruction of <3 side branches with a normal MPD
Cambridge 3 (mild) Dilatation/obstruction of >3 side branches with a normal MPD
Cambridge 4 (moderate) Cambridge 3 with stenosis/dilatation of MPD
Cambridge 5 (severe) Cambridge 3 and 4 plus additional obstructions, cysts, stenosis of the main pancreatic duct, and calculi.
FSE‑Fast Spin Echo; GRE‑Gradient Recalled Echo

206 Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019
Kamat, et al.: Imaging in chronic pancreatitis

structural information, FDG‑PET with CT and more Special varieties of CP


recently with MRI has been used to assess focal pancreatic
lesions. [60] The standardized uptake value  (SUV) of Few special varieties of CP are autoimmune pancreatitis
FDG is significantly greater in malignant masses of the and groove or paraduodenal CP.
pancreas compared with focal pancreatic masses in
CP. SUV  >4 is usually seen in a pancreatic carcinoma Autoimmune pancreatitis (AIP)
[Figure 10A and 10B], SUV of 3-4 is more commonly seen It is a rare type of CP accounting for about 2-6% of all cases of
in cases of focal pancreatic masses in CP and SUV <3 is seen CP.[65,66] It is commonly seen in association with IgG4‑related
in healthy individuals [Figure 11C and D].[61,62] However, disease and other autoimmune conditions like primary
focal lesions in autoimmune pancreatitis (AIP) have high
SUV and there is no significant difference compared with
pancreatic carcinoma.[63] Nodular FDG uptake is more
common in pancreatic carcinomas as compared with
AIP (95% versus 23.1%). AIP commonly shows longitudinal
FDG uptake  (69.2% of AIP versus 2.5% of pancreatic
carcinoma cases).[60,63] Several studies have shown the
sensitivity and specificity of FDG‑PET to be between 81
and 100% and 65 and 100%, respectively, for diagnosing
carcinoma in cases of focal pancreatic masses.[64]

A B

A B C
Figure 10 (A-C): ERCP findings in chronic pancreatitis: In a patient
with early chronic pancreatitis (A), mild dilatation of the main pancreatic
duct (arrow) and side branches (short arrow) is seen. Marked ductal
dilatation (arrow) with a dominant stricture (short arrow) is shown in B.
In another patient (C), strictures (arrow) and intraductal calculi (short
arrow) are seen

C D
Figure 11 (A-D): FDG‑PET in chronic pancreatitis: Axial PET image (A)
and corresponding coronal MIP image  (B) shows marked FDG
avidity (SUV max‑12) in the pancreatic head mass in a patient with
pancreatic adenocarcinoma. In a patient with mass forming chronic
pancreatitis show PET shows low FDG avidity in the pancreatic head
mass (arrow, C and D)

A B A B

C D
Figure 12 (A-D): Imaging features in autoimmune pancreatitis: Axial
CT image (A) shows sausage shaped pancreas (arrow). In a different
patient, CT (B) shows sausage shaped pancreas (arrow) with peripheral
hypodense rim (short arrow). MRI in the same patient (C) shows slightly
bulky sausage shaped pancreas (arrow) with hypointense rim (short Figure 13: Focal autoimmune pancreatitis: EUS demonstrated a mass
arrow). MRCP in another patient  (D) with autoimmune pancreatitis in the head of pancreas (arrow, A) with predominantly hard areas (blue
shows hilar stricture (arrow) areas, arrow, B)

Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019 207
Kamat, et al.: Imaging in chronic pancreatitis

A B

A B

Figure 15: EUS in groove pancreatitis: Thickening of the duodenal wall


with a cyst (arrow, A) is seen. The tissue in the pancreatoduodenal
groove is hard on elastography (arrow B, blue and green areas)

Adenocarcinoma in CP
There is an increased risk of adenocarcinomas in cases
of CP, however this risk is much higher with hereditary
C D and tropic pancreatitis as compared with alcohol related
Figure 14: CT findings in groove pancreatitis: Axial (A) and coronal CP.[2] CP can present as a focal mass in about 30% cases.
(B) CT images show thickening of the duodenum (arrow, A) with a Differentiation from pancreatic ductal adenocarcinoma
hypodense soft tissue in the pancreatoduodenal groove (arrow, B). is quite challenging.[35] Double duct sign may be seen
Coronal CT images (C and D) in another patient show a more pronounced
hypodense soft tissue in the pancreatoduodenal groove (arrows). Also in both the conditions.[52] Presence of calcifications and
note the dilatation of the pancreatic duct (short arrow, C) ductal calculi are more commonly associated with CP.
The mild enhancement during the arterial and a persistent
biliary cirrhosis, primary sclerosing cholangitis, Sjogren’s enhancement during the pancreatic phase are relatively
syndrome, etc.[4,41] CT shows diffuse smooth hypodense specific but not sensitive for distinguishing mass forming
enlargement of the gland with enhancement in the delayed CP from adenocarcinomas.[71] One of the important signs
phase [Figure  11A]. MRI shows reduced T1 signals and differentiating focal CP from ductal adenocarcinoma is the
mildly raised T2 signals, with delayed post‑gadolinium duct penetrating sign seen on MRCP. Here, a smoothly
enhancement. Capsule like rim of decreased intensity is stenotic duct is seen to penetrate the mass with no cutoff
a relatively specific finding [Figure 11B and 11C].[4] AIP is as commonly appreciated in an adenocarcinoma. Duct
commonly diffuse in nature and rarely focal/multifocal. penetrating sign has a sensitivity and a specificity of 85%
Important differentials are lymphomas, metastasis, and and 96%, respectively.[2]
other infiltrative disorders. Simultaneous involvement of
other systems favors a diagnosis of AIP [Figure 11D]. Focal Summary of diagnostic tests
pattern is much less common and is difficult to differentiate Sensitivities of the diagnostic tests for CP in descending
from ductal adenocarcinomas [Figure 12].[67] order are ERCP  (82%), EUS  (81%), MRCP  (78%),
MDCT  (75%), and ultrasound  (67%). Specificities for
Groove pancreatitis the diagnosis of CP are MRCP  (96%), ERCP  (94%),
In groove/paraduodenal pancreatitis, there is focal MDCT (91%), and EUS (90%). MRI, MDCT, EUS, and ERCP
inflammation in the pancreaticoduodenal groove with were found to have high diagnostic accuracy. Among
or without involvement of the head of pancreas. [68] them, the latter two had the highest scores. However, due
Obstruction of the accessory pancreatic duct is suspected to the invasive nature of these tests, MDCT and MRCP are
to be the etiology of this entity.[69] There can be ill‑defined preferred over these tests. MDCT and MRCP are the first
fat stranding to frank fibrotic soft tissue within the groove line investigation in CP. ERCP is generally used only when
showing delayed post‑contrast enhancement [Figure  13]. therapeutic interventions are planned. ERCP for diagnostic
Associated medial duodenal wall thickening and cystic foci purpose has been substituted by EUS, MDCT, and MRCP.[7]
near the minor papilla may be seen [Figure 14].[70] MRI shows
hypointensity on T1‑weighted and mild hyperintensity on Financial support and sponsorship
T2‑weighted images, with delayed enhancement. Cystic Nil.
lesions in the groove are better appreciated on T2‑weighted
images.[68] EUS and EUS elastography are also useful in Conflicts of interest
depicting changes of groove pancreatitis [Figure 15]. There are no conflicts of interest.
208 Indian Journal of Radiology and Imaging / Volume 29 / Issue 2 / April-June 2019
Kamat, et al.: Imaging in chronic pancreatitis

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