Imaging of acute pancreatitis

and its complications

 CT Findings of the Normal Pancreas
• Contrast-enhanced CT examination that is considered as the gold
standard in the evaluation of the patients with acute pancreatitis.

• Not only establishes the diagnosis of acute pancreatitis, but also

allows to stage the severity of the disease.

• Imaging of pancreatitis is optimally performed in the pancreatic

parenchymal phase (late arterial; ~ 40 seconds after contrast
injection), which is the most sensitive timing to detect subtle areas of
decreased enhancement suggestive of necrosis.
• The normal pancreas is an intermediate gray band of soft-tissue
density (~ 40 Hounsfield units) in the upper abdomen.

• When IV contrast is administered, the normal pancreas enhances

homogenously and uniformly.

• The surface of the normal pancreas has a frond-like or crenellated

appearance.
• The surrounding fat is quite black, with no inflammatory change.

• No free fluid is seen around the normal pancreas.

• Oral contrast is not needed to assess the pancreas.

 MRI Appearances
• The normal pancreas appears slightly hyperintense than the liver on
T1-weighted images due to the acinar protein content, and isointense
or slightly hypointense on T2-weighted images.

• While the pancreas is maximally enhanced at ~ 40 seconds of

intravenous gadolinium administration, it becomes isointense with
the liver in the later phases.
• Normal pancreas, CT without IV or
oral contrast, soft tissue window.
• A, Axial image. B, Close-up.
• Without oral and IV contrast, the
pancreas can be a bit harder to
identify.
• The pancreatic head is anterior to
the inferior vena cava and medial to
duodenum. The body of the
pancreas crosses the midline and
then moves posteriorly. The
pancreatic tail ends anterior to the
spleen.
• Normal pancreas, CT with IV and oral
contrast, soft tissue window.
• This scan shows a normal pancreas. In
many patients, the pancreas is not so
horizontally oriented and is therefore
difficult to see in a single slice.
• The contrast between the dark bile and
the bright pancreatic tissue is increased
by the administration of IV contrast,
because the pancreas enhances as a
result of high blood flow.
• The fat surrounding the pancreas is
dark, which is normal and indicates the
absence of inflammatory stranding—
almost the entire pancreas is outlined in
fat and has distinct border.
 Acute pancreatitis
• Acute pancreatitis is an acute inflammatory disease of the pancreas
characterized by auto-digestion of the pancreatic parenchyma,
interstitial fat necrosis and necrotizing vasculitis, resulted from the
inappropriate intracellular activation of proteolytic pancreatic
enzymes.

• The inflammatory process may be limited to the pancreas, spread to

surrounding tissues or even involve the remote organs, resulting in
multi-organ failure and occasional death.
• Pancreatitis has numerous precipitating factors, but gallstones cause
the majority of cases of acute pancreatitis.

• Alcohol is mainly responsible for chronic pancreatitis.

• Clinical symptoms and presentation vary widely and range from mild
to severe.
• Patients with milder forms present with pain, vomiting, and
abdominal tenderness.

• Those with severe forms present with shock, organ failure, and
hemorrhage.

• The severe hemorrhagic clinical signs are Grey Turner sign (flank
bruising), and Cullen sign (periumbilical bruising).

• Clinical severity is ranked by either Ranson or APACHE II criteria.

 Revised Atlanta classification (2012)
• According to the Revised Atlanta classification (RAC) 2012, the diagnosis of
AP requires two of the following three features:

• (1) abdominal pain consistent with acute pancreatitis (acute onset of a

persistent, severe, epigastric pain often radiating to the back).

• (2) serum lipase activity (or amylase activity) at least three times greater
than the upper limit of normal.

• (3) characteristic findings of acute pancreatitis on (CECT) and less

commonly (MRI) or (US).
• Patients usually meet the criteria for acute pancreatitis on the basis of
symptoms and laboratory results alone and may not require imaging
initially. (Pancreatitis is a clinical diagnosis)

• Imaging may be performed early in the disease :

In cases which the diagnosis is ambiguous,
To look for causative factors,
If the patient does not improve clinically, or
If complications are suspected.
• The ACR recommends ultrasound as the most indicated imaging test in a
first episode of pancreatitis, as a result of its ability to assess for gallstone
pancreatitis and to rule out other causes of acute abdomen.

• limitations related to paralytic ileus accompanying in the first 48 hours of

the disease.

• Pancreas may be seen normal in the cases of mild acute pancreatitis.

• Inability to make differential diagnosis of the interstitial and the necrotizing

pancreatitis.
• Contrast-enhanced CT is most commonly used to fulfill the radiologic
criterion.

• (MRI) has earned an ever more important role in the diagnosis of

acute pancreatitis. It is especially useful for imaging of patients with
iodine allergies or renal failure and the superiority in the
characterization of fluid collections .
• The (RAC) 2012 of acute pancreatitis divides the condition into :
Interstitial edematous pancreatitis (IEP), and
Necrotizing pancreatitis.

• (Formerly termed mild and severe acute pancreatitis).

• This morphological classification system is based on findings on

contrast-enhanced CT.
 Interstitial edematous pancreatitis
• IEP constitutes 90–95% of cases of acute pancreatitis.

• It is histologically characterized by interstitial edema.

• Usually limits itself within 48 to 72 hours.

• Gives a rapid response to the conservative treatment.

• Organ failure and local complications are generally not observed.

• Progression to the severe form is quite rare.

• The ultrasound appearances may be entirely normal but common
findings may include generalized (or less commonly, focal)
enlargement of the gland with reduced reflectivity.

• The pancreatic margins may be difficult to define and peri-pancreatic

fluid may be visualised.
• CECT findings in (IEP) include :

Focal or diffuse enlargement of the gland,

Ill defined parenchymal contours,
Decreased parenchymal density,
Normal homogeneous enhancement or slightly heterogeneous enhancement of
the pancreatic parenchyma, which is attributable to edema.
Fluid collections in the peri-pancreatic region.
Increased attenuation of the peri-pancreatic fat tissue ‘‘fat stranding’’.
• Interstitial edematous pancreatitis:

• US image, obtained at admission,

reveals enlargement and decreased
parenchymal echogenicity of the
whole pancreas (P) with poorly
defined contours due to interstitial
edema.

• Note also a small amount of peri-

pancreatic fluid.
• Focal interstitial edematous
pancreatitis :
• US image, obtained at
admission, shows focal
hypoechoic areas (arrows)
in the pancreas (P) due to
interstitial edema.
• There is a small amount of
peripancreatic fluid.
• Interstitial edematous
pancreatitis in patient with
gallstones:
• Contrast-enhanced CT
image, performed 3 days
after onset of acute attack,
reveals enlargement,
diffusely decreased
parenchymal density and
loss of normal lobular
contour of the pancreas (P)
due to interstitial edema.
• Acute peri-pancreatic fluid
collection and numerous
gallstones (arrow) in the
gallbladder are also seen.
• Interstitial edematous :
• Contrast-enhanced CT
image performed 3 days
after onset of acute attack,
shows extensive stranding
of peri-pancreatic fat
(arrows), acute
peripancreatic fluid
collection (F) extending to
left anterior pararenal
space and thickening of the
left Gerota fascia (P:
pancreas).
 Necrotizing pancreatitis
• Necrotizing pancreatitis accounts for 5%–10% of cases.

• Pancreatic parenchymal necrosis, developing as a result of the thrombosis

of the pancreatic microcirculation.

• Defined as diffuse or focal areas of non-viable pancreatic parenchyma that

typically are associated with peri-pancreatic fat necrosis.

• In general, it emerges 24-48 hours after the onset of acute attack and it is
usually well established with contrast enhanced CT or MRI performed 72
hours after the onset of acute attack.
• The Revised Atlanta classification system distinguishes three forms of
acute necrotizing pancreatitis, depending on location:

Pancreatic parenchymal necrosis alone,

Peri-pancreatic fat tissue necrosis alone, and
Combined necrosis.
 Pancreatic parenchymal necrosis
• Pancreatic parenchymal necrosis alone seen in fewer than 5%
patients and usually involves the body or the tail of the pancreas.

• Contrast enhanced CT demonstrates necrosis as a more

homogeneous non-enhancing area and, later in the course of the
disease, as a more heterogenous area.

• This is the result of a process in which the non-viable and necrotic

tissues slowly begin to liquefy.
 Peri-pancreatic fat tissue necrosis
• Approximately 20% of patients, with only peri-pancreatic fat tissue
necrosis.

• The pancreas enhances normally.

• Its presence is diagnosed when peripancreatic tissues shows heterogenous

areas of non-enhencement.

• All heterogeneous peri-pancreatic collections should be considered as

areas of fat tissue necrosis unless proven otherwise.
 Combined Necrosis
• The combined subtype is the most common, accounting for 75% of
cases.

• Characterised on imaging by a combination of imaging features

observed in the other 2 types.

• Nonenhancing pancreatic parenchyma, as well as nonenhancing

heterogeneous peripancreatic collections, and typically accumulating
in the lesser sac and anterior pararenal space.
• Pancreatic necrosis :
• Contrast enhanced CT
image at the portal
venous phase, obtained 3
days after the onset of
acute attack, show full
width necrosis (N) of the
pancreatic neck, body
and proximal tail.
• Parenchyma of the distal
tail is seen to enhance
normally.
• Pancreatic necrosis (> 75%) in a patient with gallstones.
• Contrast-enhanced CT images at the portal venous phase (a,b), obtained 3 days after the onset of
acute attack, show full width necrosis (N) of the pancreatic neck, body and proximal tail.
• Parenchyma of the head and distal tail is seen to enhance normally.
• Fluid collection (F) extending to left anterior para-renal space, thickening of the left Gerota fascia,
and a gallstone (arrow) in the gallbladder are also seen (P: pancreas).
• Focal pancreatic necrosis (< 30%) in a patient with gallstones.
• Contrast-enhanced CT images at the portal venous phase (a, b), obtained 3 days after the
onset of acute attack, reveal focal non-enhancing areas of pancreatic necrosis (short
white arrows) in the head of the pancreas (P).
• There are fluid collection (F) and thickening of the posterior parietal peritoneum (long
white arrow) due to inflammation.
 Pancreatic and Peripancreatic Collections

• Acute pancreatitis can be accompanied by pancreatic parenchymal or

peripancreatic collections.

• The Revised Atlanta classification makes an important distinction

between collections based on the time course (≤4 weeks or >4 weeks
from onset of pain) and the presence or absence of necrosis at
imaging.
 Acute peri-pancreatic fluid collections
• APFC is a collection of enzyme-rich pancreatic juice predominantly
collected adjacent to the pancreas.

• This collection usually develops within the first 48 hours in patients

with IEP.

• They are resulted from pancreatic and peri-pancreatic inflammation

or by rupture of one or more small peripheral pancreatic side duct
branches.
• APFCs contain only fluid and are visualized as homogeneous fluid-
attenuation collections that lack a wall and tend to conform to the
retroperitoneal spaces.

• APFCs are always peri-pancreatic in location.

• If a similar-appearing collection is seen within the pancreatic parenchyma,

the diagnosis is no longer IEP.

• Most APFCs remain sterile and resolve spontaneously, and drainage should
be not be performed because of the risk of infection.
• Interstitial edematous
pancreatitis :

• Contrast enhanced CT
image obtained at
admission, reveals
heterogeneous
enhancement of the
pancreatic paranchyma
due to edema.

• Acute peripancreatic fluid

collection(F)
predominantly collected
in the left anterior
pararenal space
(P:pancreas).
 Pancreatic Pseudocyst
• If an APFC has not resolved after 4 weeks, it becomes more organized and
develops pseudocyst.

• Pancreatic pseudocyst is defined as a fluid collection of pancreatic juice

enclosed by a non-epithelialised wall of fibrous or granulation tissue.

• It should contain only fluid.

• If there is even a small area of fat or soft-tissue attenuation in an otherwise

fluid-attenuation collection, the diagnosis is not pseudocyst.
• Pseudocysts are most frequently developed in the lesser sac,
although they may be seen anywhere from the mediastinum to the
pelvis.

• On contrast enhanced CT, pseudocysts are usually seen as a thin-

walled, round- or oval-shaped cystic lesion with a density < 20 HU
with peripheral wall enhancement.

• At MR imaging, pseudocysts are uniformly hyperintense on T2-

weighted images, with no solid components or debris in the fluid.
• Approximately 50% of the pseudocysts are asymptomatic and resolve
spontaneously.

• Pseudocysts should be treated with percutaneous or endoscopic

drainage or surgically; if they are :
Symptomatic,
Their size is over 5 cm or gradually increasing, and
Persist longer than 6 weeks.
• Infected (supurative) pseudocyst is the new name for what had been
described in the Atlanta Symposium as a pancreatic abscess.

• An infected pseudocyst is a well-circumscribed, pus containing,

encapsulated fluid collection near the pancreas.

• On contrast enhanced CT images, the wall of the infected pseudocyst is

thicker and more irregular than that of a sterile pseudocyst.

• Air bubbles or air-fluid level may be seen within the pseudocyst in 20% of
the patients.
• Interstitial edematous
pancreatitis :
• Contrast enhanced CT
image, obtained 6
weeks after the onset
of acute attack,
reveals a pseudocyst
(Ps) in the
gastrohepatic
ligament.
• Interstitial edematous
pancreatitis :
• T2-weighted MR
image, obtained 6
weeks after the onset
of acute attack,
reveals a pseudocyst
(Ps) (P: pancreas).
• An infected pseudocyst
(Ps).
• Contrast enhanced CT
image, obtained 8 weeks
after the onset of acute
attack, reveals an
encapsulated, rounded
fluid collection (Ps) with
septations and a thick and
irregular wall increased
contrast enhancement.
• Note air bubbles within
the pseudocyst (P:
pancreas).
 Acute necrotic collections
• ANCs are present within the first 4 weeks of symptom onset as poorly
organized necrotic collections that occur only in necrotizing
pancreatitis.

• Develops as a result of the pancreatic glandular and/or peri-

pancreatic fatty tissue necrosis to become liquefied.

• ANCs are often found in the lesser sac and para-renal spaces and may
extend into the pancreas within areas of parenchymal necrosis.
• ANCs typically demonstrate a variable amount of fluid and can be
distinguished from APFCs by the presence of non-liquefied (solid)
debris, such as fat globules within the fluid.

• The presence of fat attenuation within a collection at non-enhanced

CT is helpful for identifying necrosis and diagnosing ANCs.

• Any peripancreatic collection associated with known pancreatic

parenchymal necrosis should be termed an ANC, even if it is
homogeneous and contains no non-liquefied debris.
• Necrotizing acute pancreatitis
in a patient with gallstones.
• Contrast enhanced CT images
(a) obtained 3 weeks after the
onset of acute attack reveal a
post-necrotic
pancreatic/peripancreatic
fluid collection (PNPFC)
contained solid necrotic
debris.
• Note the hyperdense stones in
the gallbladder(long arrow)
and common bile duct (short
arrow) (P: pancreas).
 Walled-Off Necrosis
• Similar to the development of a pseudocyst from APFC over the time.

• WON evolves from the ANC, and results in a non-epithelialised thick

wall developed between the necrosis and the adjacent viable tissue
after 4 weeks.

• WON is an irregular, partially liquefied collection, which may contain

solid necrotic debris and may expand to the peripancreatic space.
• May involve the pancreatic parenchymal tissue and/or peri-pancreatic
tissue.

• Solid components in these collections are identified better on US and

T2-weighted MR images than on CT.

• WON may be mistaken for pseudocysts, and the existence or non-

existence of necrosis to on the CT performed in the beginning of
acute pancreatitis, and clinical course enables to differentiate the
WON from a pseudocyst.
• Findings that are in favour of WOPN include :
Having a larger size,
Extension to the paracolic or retrocolic spaces,
Irregular wall definition,
Presence of solid or fat attenuation debris,
Presence of pancreatic parenchymal deformity and discontinuity.

• Ideal treatment of WOPN is controversial and most centers prefer the

treatment with operative necro-sectomy in the infected or symptomatic
cases.
 Infected necrosis
• Any collection can be sterile or infected, although infection occurs far
more frequently in necrotic collections.

• Clinically, infection is suspected in a previously stable patient who

experiences decompensation with signs of infection.

• The only imaging finding of an infected collection is the presence of

gas within the collection.
• Wall enhancement is not a reliable indicator of infection, since it is
invariably present in mature collections (pseudocyst and WON).

• An infected pseudocyst still lacks solid components that, if present,

should instead lead to the diagnosis of infected WON.

• The gas often appears as multiple small bubbles scattered throughout

the collection owing to the complex nature of necrotic collections
• Necrotizing acute pancreatitis in a patient with gallstones.
• Contrast enhanced CT images (a) obtained 3 weeks after the onset of acute attack reveal a post-
necrotic pancreatic/peripancreatic fluid collection (PNPFC) contained solid necrotic debris.
• A follow-up contrast enhanced CT images (b), obtained 6 weeks after the onset of acute attack,
show an encapsulated walled off pancreatic necrosis(WON), evolving from PNPFC.
• Note the hyperdense stones in the gallbladder(long arrow) and common bile duct (short arrow)
(P: pancreas).
• Walled off pancreatic
necrosis (WOPN) in a
patient with alcoholic
acute pancreatitis.
• Contrast enhanced CT
image, obtained 8 weeks
after the onset of acute
attack, shows a WON
with an enhanced
irregular thick wall and
contained necrotic fatty
tissue.
• Evolution of necrotizing pancreatitis during 2
months.
• (a) Week 1: Axial contrast enhanced CT
image shows a necrotic pancreatic neck (*).
• (b) Week 2: Axial contrast-enhanced CT
image shows a new heterogeneous necrotic
peripancreatic collection (arrow) that is
inseparable from the pancreatic necrotic
collection (*); both findings are consistent
with an ANC.
• (c) Week 3: Axial non-enhanced T2-weighted
MR image better shows the contents of the
ANC (*), including hyperintense fluid and
non-liquefied debris, including necrotic
pancreatic neck and body (arrow). Note the
developing partial wall.
• (d) Week 5: Axial contrast-enhanced CT
image shows maturation of the wall and a
more round appearance of what is now
referred to as WON (*).
• Necrotizing pancreatitis:
• (a) Axial contrast-enhanced CT image obtained in week 3 shows the pancreatic tail (*)
and a peri-pancreatic ANC containing non-liquefied debris with foci of fat attenuation
(arrows).
• (b) Axial contrast-enhanced CT image obtained in week 6 because the patient
experienced decompensation and was readmitted shows organization of the collection
(*) with multiple new foci of gas, findings that are consistent with infected WON.
 Vascular cimplications
• Vascular complications occur in 25% of patients with acute
pancreatitis.

• The most common complications are :

Thrombosis of the portal venous system,
Hemorrhage related to the erosion in arteries of the upper
gastrointestinal system, and
Pseudoaneurysm development.
• Splenic vein thrombosis is the most common complication of acute
pancreatitis and results from the inflammatory intimal injury or the
external compression by fluid collections.

• This may result in portal hypertension, variceal development and

splenic infarction in long term.

• Although rare, thrombosis of portal vein or superior mesenteric vein

may also be seen.
• Walled off pancreatic
necrosis (WON) and
venous thrombosis in a
patient with alcoholic
acute pancreatitis.
• Contrast enhanced CT
image at the portal
venous phase, obtained 8
weeks after the onset of
acute attack, shows a
multiloculated WON with
an enhanced irregular
thick wall.
• Note the filling defects in
the main portal vein
consistent with thrombus
(arrow).
• Spontaneous arterial hemorrhage in acute pancreatitisis a rare, but crucial
complication.

• Erosion of pancreatic or peripancreatic arteries by the proteolytic enzymes

may result in a free hemorrhage or pseudoaneurysm devel-opment.

• The most commonly affected arteries are :

• Splenic artery (40%),
• Gastroduodenal artery(30%), and
• Pancreaticoduodenal artery (20%).
• Intracystic hemorrhage in patient with an idiopathic recurrent acute pancreatitis.
• Contrast enhanced CT images at the arterial (a) and portal venous (b) phases reveal :
• Active hemorrhage into the pseudocyst (Ps) from the common hepatic artery
(blackarrow).
• High attenuation fluid (F) consistent with free intra-abdominal hemorrhage is also seen.
• Note a filling defect in the splenic vein due to a thrombus (white arrow).