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GASTROINTESTINAL
IMAGING
675
Revised Atlanta Classification for
Acute Pancreatitis: A Pictorial Essay1
The 2012 revised Atlanta classification is an update of the original
1992 Atlanta classification, a standardized clinical and radiologic
nomenclature for acute pancreatitis and associated complications
based on research advances made over the past 2 decades. Acute
pancreatitis is now divided into two distinct subtypes, necrotizing
pancreatitis and interstitial edematous pancreatitis (IEP), based on
the presence or absence of necrosis, respectively.The revised clas-
sification system also updates confusing and sometimes inaccurate
terminology that was previously used to describe pancreatic and
peripancreatic collections. As such, use of the terms acute pseudo-
cyst and pancreatic abscess is now discouraged. Instead, four distinct
collection subtypes are identified on the basis of the presence of
pancreatic necrosis and time elapsed since the onset of pancreatitis.
Acute peripancreatic fluid collections (APFCs) and pseudocysts
occur in IEP and contain fluid only. Acute necrotic collections
(ANCs) and walled-off necrosis (WON) occur only in patients with
necrotizing pancreatitis and contain variable amounts of fluid and
necrotic debris. APFCs and ANCs occur within 4 weeks of disease
onset. After this time, APFCs or ANCs may either resolve or per-
sist, developing a mature wall to become a pseudocyst or aWON,
respectively. Any collection subtype may become infected and man-
ifest as internal gas, though this occurs most commonly in necrotic
collections. In this review, the authors present a practical image-rich
guide to the revised Atlanta classification system, with the goal of
fostering implementation of the revised system into radiology prac-
tice, thereby facilitating accurate communication among clinicians
and reinforcing the radiologist’s role as a key member of a multidis-
ciplinary team in treating patients with acute pancreatitis.
©
RSNA, 2016 • radiographics.rsna.org
Bryan R. Foster, MD
Kyle K. Jensen, MD
Gene Bakis, MD
Akram M. Shaaban, MBBCh
FergusV
. Coakley, MD
Abbreviations: ANC = acute necrotic collec-
tion, APFC = acute peripancreatic fluid collec-
tion, IEP = interstitial edematous pancreatitis,
WON = walled-off necrosis
RadioGraphics 2016; 36:675–687
Published online 10.1148/rg.2016150097
Content Codes:
1
From the Department of Diagnostic Radiol-
ogy, Oregon Health & Science University, 3181
SW Sam Jackson Park Rd, Portland, OR 97239
(B.R.F., K.K.J., G.B., F.V.C.); and Department
of Radiology, University of Utah, Salt Lake City,
Utah (A.M.S.). Presented as an education ex-
hibit at the 2014 RSNA Annual Meeting. Re-
ceived April 6, 2015; revision requested June 30
and received August 10; accepted August 31. For
this journal-based SA-CME activity, the authors,
editor, and reviewers have disclosed no relevant
relationships. Address correspondence to
B.R.F. (e-mail: fosterbr@ohsu.edu).
©
RSNA, 2016
After completing this journal-based SA-CME
activity, participants will be able to:
■ Discuss the revised Atlanta classifica-
tion system.
■ Distinguish interstitial edematous pan-
creatitis from necrotizing pancreatitis at
imaging.
■ Describe the imaging appearance of
pancreatitis-associated collections, in-
cluding acute peripancreatic fluid collec-
tions, pseudocysts, acute necrotic collec-
tions, and walled-off necrosis.
See www.rsna.org/education/search/RG.
SA-CME LEARNING OBJECTIVES
Introduction
Beginning in 2007, the Acute Pancreatitis Classification Working
Group polled an international cohort of pancreatic experts, includ-
ing 11 pancreatic societies, with the goal of revising the original 1992
Atlanta classification system for acute pancreatitis (1,2). Although
the original Atlanta classification system established common terms
for acute pancreatitis and related complications, the nomenclature
proved to be confusing, leading to incorrect use of terms in both
clinical practice and research. In addition, advances in imaging and
in the understanding of pathophysiology necessitated substantial
revision of the classification system (2). A draft was posted on the
Pancreas Club Web site in 2008 (3).This draft was referrenced in
several initial publications in the radiology literature (4–6). After a
total of four Web-based revisions, the revised Atlanta classification
system was finalized in 2012 and published shortly thereafter, with
updates to the earlier-cited draft (2).
An earlier
incorrect version
of this article
appeared online.
This article was
corrected on
March 28, 2019.
This copy is for personal use only. To order printed copies, contact reprints@rsna.org
676  May-June 2016	 radiographics.rsna.org
recognized by the working group that previously
used terms such as acute pseudocyst and pancreatic
abscess were confusing and had fallen out of favor,
in addition to their not being entirely descriptive
of the pathologic condition.Therefore, a specific
lexicon was needed to distinguish necrotic from
nonnecrotic collections (7). Use of standardized
reporting schemas and application of a well-
defined lexicon to a specific disease are thought
to be important for effective communication
and quality care and are in fact becoming more
common in everyday radiologic practice (8,9).
Most important, adoption of such standardized
terminology allows the radiologist to be an effec-
tive member of a multidisciplinary team in the
diagnosis and treatment of acute pancreatitis.
The purpose of this article is to serve as an im-
age-rich practical overview of the revised Atlanta
classification system such that the radiologist
will have a working understanding of the system
and can immediately incorporate the lexicon
into clinical practice.To that end, we focus on
key imaging characteristics that help differenti-
ate collections that often have a similar appear-
ance, describe various infectious complications,
and discuss imaging pitfalls. In addition, we will
propose a reporting schema to facilitate accurate
communication.
Acute Pancreatitis: Over-
view and New Diagnostic Criteria
Acute pancreatitis is an acute inflammatory
condition, with a range of severity as well as vari-
ous local and systemic complications. Gallstones
and alcohol are the first and second most com-
mon causes of acute pancreatitis, respectively,
and additional variants occur when patients are
stratified by sex. In 2009, acute pancreatitis was
the most common cause of hospital admission
for gastrointestinal disorders in the United States,
with approximately 275 000 admissions, nearly
double the number in the previous decade.This
increase is thought to be secondary not only to
nationwide increases in obesity and the incidence
of gallstones, but also to more sensitive and more
frequently used laboratory testing (10). A majority
of patients have mild acute pancreatitis, which car-
ries essentially no risk of mortality. In the subset of
patients with organ failure (severe disease) or in-
fected necrosis, however, the mortality rate reaches
30% (2,11).The revised Atlanta classification
requires that two or more of the following crite-
ria be met for the diagnosis of acute pancreatitis:
(a) abdominal pain suggestive of pancreatitis, (b)
serum amylase or lipase level greater than three
times the upper normal value, or (c) characteristic
imaging findings (2). Contrast material–enhanced
CT is most commonly used to fulfill the radiologic
One major component of the revised classifi-
cation system that is of particular importance to
radiologists is the manner in which pancreatitis-
associated collections (local complications) are
described and named (Table 1). It was well
TEACHING POINTS
■
■ In the 1st week after the onset of pancreatitis, imaging findings
correlate poorly with clinical severity, and imaging sensitivity
for necrotizing pancreatitis is decreased in the first few days. In
addition, any local complications that are detected in the 1st
week generally do not necessitate intervention because treat-
ment is based on supportive measures and management of or-
gan failure. Initial imaging is most useful when performed 5–7
days after hospital admission, when local complications have
developed and pancreatic necrosis (if present) should be clearly
distinguishable.
■
■ In the revised classification system, new definitions were cre-
ated to clearly stratify acute pancreatitis into two subcategories
based on imaging findings: IEP and necrotizing pancreatitis.
IEP is more common and represents nonnecrotizing inflam-
mation of the pancreas. The entire pancreas will enhance at
contrast-enhanced CT or MR imaging, with no unenhanced
(necrotic) areas, although enhancement of the gland may be
less avid than that of the normal pancreas owing to interstitial
edema. IEP usually manifests with focal or diffuse pancreatic
enlargement and is typically surrounded by wispy peripancre-
atic inflammation or a small amount of fluid. In addition, there
should be no surrounding peripancreatic necrotic collections
in IEP, although there may be surrounding fluid-containing
collections. Necrotizing pancreatitis accounts for 5%–10% of
cases of acute pancreatitis. It is important to understand that
necrosis may involve either the pancreatic parenchyma or the
peripancreatic tissues and in both cases is termed necrotizing
pancreatitis. There are three subtypes of necrotizing pancreati-
tis; the subtypes are based on the anatomic area of necrotic
involvement: (a) pancreatic only, (b) peripancreatic only, and
(c) combined pancreatic and peripancreatic.
■
■ The revised Atlanta classification makes an important distinc-
tion between collections that contain purely fluid (those en-
countered in nonnecrotizing pancreatitis and IEP) and collec-
tions that contain necrotic debris in addition to fluid (those
encountered in necrotizing pancreatitis). The terms acute
pseudocyst and pancreatic abscess have been abandoned.
Similarly, the use of the term pseudocyst in radiology reporting
to describe any pancreatitis-related collection is misleading to
treating physicians, since the term implies that these collections
always contain purely fluid, which is not the case in necrotic
collections. Instead, the revised classification includes new defi-
nitions that more accurately describe the various types of col-
lections encountered: APFC, pseudocyst, ANC, and WON. The
important distinctions for classifying collections correctly are the
time course (≤4 weeks or >4 weeks from onset of pain) and the
presence or absence of necrosis at imaging.
■
■ If an APFC has not resolved within 4 weeks, it becomes more
organized, with development of a capsule that manifests as
an enhancing wall at contrast-enhanced CT. At this point, the
collection is referred to as a pseudocyst, and, since there is no
necrosis, it should contain only fluid with no nonliquefied com-
ponents. If there is even a small area of fat or soft-tissue attenu-
ation in an otherwise fluid-attenuation collection, the diagnosis
is not pseudocyst but WON.
■
■ Any collection can be sterile or infected, although infection oc-
curs far more frequently in necrotic collections. Clinically, infec-
tion 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).
RG  •  Volume 36  Number 3	 Foster et al  677
patients as having either severe or mild pancreati-
tis on the basis of the presence or absence of or-
gan failure, respectively (1). However, emerging
evidence indicated that a large subset of patients
with local complications experienced substantial
morbidity but little mortality (11).Therefore, a
third category was added to the new classifica-
tion—moderately severe acute pancreatitis—to
describe this patient group (2). Organ failure and
local complications are not seen in patients with
mild pancreatitis, who are usually discharged
within the 1st week, with very low mortality
(13).These patients rarely require CT for local
complications, and imaging may be useful only
in assessing the cause of pancreatitis (eg, ultraso-
nography [US] or MR cholangiopancreatography
for choledocholithiasis) (12).
Moderately severe acute pancreatitis manifests
in patients with transient organ failure lasting less
than 48 hours and/or local or systemic complica-
tions. Systemic complications are generally co-
morbidities exacerbated by pancreatitis, such as
acute kidney injury in the setting of chronic renal
failure. Local complications include a variety of
pancreatic and peripancreatic collections. Such
collections generally develop in the 2nd week
(the late phase of pancreatitis) and are clinically
suspected in patients with unremitting or recur-
rent pain, a secondary peak in pancreatic enzyme
levels, worsening organ dysfunction, or sepsis
(2).These symptoms should prompt imaging
studies such as (in order of preference) contrast-
enhanced CT, contrast-enhanced MR imaging,
or unenhanced MR imaging (12).
Severe disease is characterized by organ failure
that persists for more than 48 hours. Because
criterion, but magnetic resonance (MR) imaging
is also appropriate. Although many patients will
meet the criteria for acute pancreatitis on the basis
of symptoms and laboratory results alone and may
not require imaging initially, imaging may be per-
formed early in the disease course when the cause
of the disease is unclear, to look for causative
factors such as choledocholithiasis and pancreatic
cancer. Imaging for the diagnosis of pancreatitis
is also appropriate when abdominal pain suggests
pancreatitis but the amylase or lipase level is not
elevated to the threshold value, which is often the
case at delayed presentation (12).The onset of
pancreatitis is considered to coincide with the 1st
day of pain, not the day on which the patient pres-
ents for care or the day of hospital admission (2).
Phases of Acute Pancreatitis
In pathophysiologic terms, acute pancreatitis is
divided into early and late phases.The early phase
occurs in the 1st week after onset, with the disease
manifesting as a systemic inflammatory response.
At this time, clinical severity and treatment are
mainly determined on the basis of type and degree
of organ failure.The late phase, which generally
starts in the 2nd week and can last for weeks to
months, occurs only in patients with moderately
severe or severe pancreatitis, as defined by persis-
tent organ failure and by local complications (2).
Grading of
Severity of Acute Pancreatitis
To improve the stratification of patients at the
time of presentation, the pancreatitis severity
scale was updated in the revised Atlanta clas-
sification.The original classification categorized
Table 1: Pancreatic and Peripancreatic Collections
Collection
Time after Onset
of Pain (wk)
Pancreatitis
Subcategory Location Imaging Features
APFC 4 IEP Extrapancreatic Homogeneous, fluid attenuation, con-
forms to retroperitoneal structures,
no wall
ANC 4 Necrotizing
pancreatitis
Intra- and/or extra-
pancreatic
Inhomogeneous*, nonliquefied com-
ponents†, no wall
Pseudocyst >4 IEP Extrapancreatic‡ Homogeneous, fluid filled, circum-
scribed, encapsulated with wall
WON >4 Necrotizing
pancreatitis
Intra- and/or extra-
pancreatic
Inhomogeneous, nonliquefied compo-
nents, encapsulated with wall
Sources.—References 2–4.
Note.—Any collection may become infected. ANC = acute necrotic collection, APFC = acute peripancreatic
fluid collection, IEP = interstitial edematous pancreatitis, WON = walled-off necrosis.
*Early ANCs may be homogeneous; follow-up computed tomography (CT) performed in 2nd week may help
clarify status.
†Includes solid-appearing components or fat globules within fluid.
‡Rarely, persistent pancreatic leak or disconnected duct may lead to intrapancreatic pseudocyst.
678  May-June 2016	 radiographics.rsna.org
organ failure plays a key role in determining
disease severity, an accurate definition is essential
for clinical management of acute pancreatitis.
The modified Marshall scoring system (Table 2)
is endorsed in the revised Atlanta classification
as the primary method for determining organ
failure.The modified Marshall scoring system
incorporates measurements from the respiratory,
cardiovascular, and renal systems, with a score
of 2 or higher for any system indicating organ
failure (2,14). In the 1st week after the onset of
pancreatitis, imaging findings correlate poorly
with clinical severity, and imaging sensitivity for
necrotizing pancreatitis is decreased in the first
few days (2). In addition, any local complications
detected in the 1st week generally do not neces-
sitate intervention because treatment is based on
supportive measures and management of organ
failure (15). Initial imaging is most useful when
performed 5–7 days after hospital admission,
when local complications have developed and
pancreatic necrosis (if present) should be clearly
distinguishable (2).
IEP versus
Necrotizing Pancreatitis
In the revised classification system, new defini-
tions were created to clearly stratify acute pan-
creatitis into two subcategories based on imaging
findings: IEP and necrotizing pancreatitis. IEP
is more common and represents nonnecrotiz-
ing inflammation of the pancreas.The entire
pancreas will enhance at contrast-enhanced CT
or MR imaging, with no unenhanced (necrotic)
areas, although enhancement of the gland may
be less avid than that of the normal pancreas
owing to interstitial edema. IEP usually manifests
with focal or diffuse pancreatic enlargement and
is typically surrounded by wispy peripancreatic
inflammation or a small amount of fluid (Fig 1).
In addition, there should be no surrounding peri-
pancreatic necrotic collections in IEP, although
there may be surrounding fluid-containing collec-
tions (Fig 2).
Necrotizing pancreatitis accounts for 5%–10%
of cases of acute pancreatitis (2). It is important
to understand that necrosis may involve either
the pancreatic parenchyma or the peripancreatic
tissues and in both cases is termed necrotizing
pancreatitis. There are three subtypes of necro-
tizing pancreatitis; the subtypes are based on
the anatomic area of necrotic involvement: (a)
pancreatic only, (b) peripancreatic only, and (c)
combined pancreatic and peripancreatic. The
latter subtype is the most common, accounting
for 75% of cases.The combined subtype dem-
onstrates nonenhancing pancreatic parenchyma,
as well as nonenhancing heterogeneous peripan-
creatic collections, and typically accumulating in
the lesser sac and anterior pararenal space (Fig
3a). Peripancreatic necrosis alone, in which the
pancreas enhances normally but the peripan-
creatic tissues show necrosis, with collections
containing variable amounts of fluid and nonliq-
Table 2: Modified Marshall Scoring System
Organ System Score 0 Score 1 Score 2 Score 3 Score 4
Respiratory* >400 301–400 201–300 101–200 100
Renal: serum creati-
nine (mg/dL)
1.4 1.5–1.8 1.9–3.5 3.6–4.9 5
Cardiovascular: sys-
tolic blood pressure
(mm Hg)
>90 <90, responding
to fluid resusci-
tation
<90, not respond-
ing to fluid resus-
citation
<90 with pH
<7.3
<90 with pH
<7.2
Sources.—References 2,4,14.
Note.—A score of 2 or higher indicates organ failure, with transient failure lasting less than 48 hours and persis-
tent failure lasting more than 48 hours.
*Partial pressure of oxygen/fraction of inspired oxygen, or Pao2
/Fio2
.
Figure 1.  IEP in a 28-year-old man with
alcohol-related pancreatitis. Axial con-
trast-enhanced CT image shows wispy
peripancreatic inflammation (arrows)
with normal pancreatic enhancement and
no collections.
RG  •  Volume 36  Number 3	 Foster et al  679
uefied components, occurs in 20% of cases (Fig
3b). Pancreatic necrosis alone is the least com-
mon subtype, occurring in 5% of cases, and lacks
peripancreatic collections (Fig 3c).When imaging
is performed within the first few days of disease
onset, necrosis may not be detected because the
pancreas can appear edematous and globally
or focally hypoenhancing and, as such, may be
indistinguishable from IEP. In these cases, repeat
Figure 2.  IEP in a 43-year-old
man. Axial contrast-enhanced
CT image shows peripan-
creatic inflammation (black
arrow) and a homogeneous
fluid-attenuation collection
in the left anterior pararenal
space (white arrow), a finding
that is consistent with APFC.
Figure 3.  Subtypes of necrotizing pancreatitis on
axial contrast-enhanced CT images. (a) Image of
combined pancreatic and peripancreatic necrosis
in a 58-year-old woman shows nonenhancement of
the body (*), normal enhancement of the pancreatic
tail (black arrow), and a large ANC in the lesser sac
(white arrows). (b) Image of peripancreatic necrosis
alone in an 18-year-old man shows a large, complex,
heterogeneous peripancreatic collection (arrows)
containing both fluid attenuation and nonliquefied
components, consistent with an ANC. Note normal
enhancement of the pancreatic parenchyma (*), in-
dicative of lack of pancreatic parenchymal necrosis.
(c) Image of pancreatic necrosis alone in a 33-year-
old man shows a large area of encapsulated fat and
nonenhancing pancreatic parenchyma (*), defined
as WON. Note a very small amount of residual en-
hancing parenchyma at the periphery (arrows).
contrast-enhanced CT performed 5–7 days later
is more accurate for the diagnosis of necrotizing
pancreatitis (2). In general, routine contrast-
enhanced CT is adequate for diagnosis, and
pancreatic protocol multiphase imaging (arterial
and portal phase) is typically unnecessary. If renal
failure prevents administration of intravenous
contrast material, nonenhanced MR imaging is
preferred to nonenhanced CT, although limited
availability and the difficulty of imaging criti-
cally ill patients are significant limitations of MR
680  May-June 2016	 radiographics.rsna.org
Figure 4.  IEP with APFCs on axial contrast-enhanced CT images in a 49-year-old man. (a) One day after the
onset of pain, IEP is seen with a small, homogeneous, fluid-attenuation collection in the left anterior pararenal
space (arrow). The pancreas demonstrates normal enhancement. (b–d) At 10 days after onset of pain, multiple
homogeneous fluid collections (*) can be seen in the lesser sac (b) and peripancreatic (c) and bilateral anterior
pararenal spaces (d), findings consistent with APFCs. Arrow on c = normally enhancing pancreatic tail.
imaging, and nonenhanced CT may be easier in
practice (12).
Pancreatic and
Peripancreatic Collections
The revised Atlanta classification makes an
important distinction between collections that
contain purely fluid (those encountered in IEP)
and collections that contain necrotic debris in
addition to fluid (those encountered in necrotiz-
ing pancreatitis).The terms acute pseudocyst and
pancreatic abscess have been abandoned. Similarly,
the use of the term pseudocyst in radiology report-
ing to describe any pancreatitis-related collection
is misleading to treating physicians, since the
term implies that these collections always contain
purely fluid, which is not the case in necrotic
collections. Instead, the revised classification
includes new definitions that more accurately
describe the various types of collections encoun-
tered: APFC, pseudocyst, ANC, and WON.The
important distinctions for classifying collections
correctly are the time course (4 weeks or >4
weeks from onset of pain) and the presence or
absence of necrosis at imaging (Table 1) (2).
APFC and Pseudocyst
APFCs occur during the first 4 weeks and are
present only in patients with IEP. Because the
pathogenesis involves inflammation without
necrosis, APFCs contain only fluid and are visu-
alized as homogeneous fluid-attenuation collec-
tions that lack a wall and tend to conform to the
retroperitoneal spaces (Fig 4). APFCs are always
peripancreatic in location. If a similar-appearing
collection is seen within the pancreatic paren-
chyma, it is by definition an ANC, and the diag-
nosis is no longer IEP but necrotizing pancreatitis
(2). Most APFCs resolve spontaneously, and
drainage should be not be performed because of
the risk of infecting an otherwise sterile collec-
tion (16). Just as some cases of IEP and necrotiz-
ing pancreatitis can be difficult to distinguish at
contrast-enhanced CT during the 1st week, it
may also be difficult to distinguish between an
APFC and an ANC. In general, repeat imaging at
RG  •  Volume 36  Number 3	 Foster et al  681
Figure 7.  Pseudocyst in a 55-year-old woman with
disconnected duct syndrome. Coronal two-dimensional
MR cholangiopancreatographic image shows a large
bilobed peripancreatic and intrapancreatic pseudocyst
(*) that communicates with the pancreatic tail duct (ar-
row), which is mildly dilated. Note the disconnection
of the tail duct from the ampulla owing to segmental
pancreatic body necrosis.
Figure 6.  Pseudocyst in a 48-year-old woman. Coro-
nal T2-weighted MR image obtained 8 weeks after
onset of pancreatitis shows a large homogeneous col-
lection in the lesser sac (*) with uniformly hyperintense
fluid signal and no necrotic components, findings that
are consistent with pseudocyst.
Figure 5.  Pseudocyst in a 36-year-old man. Axial CT
image obtained 6 weeks after onset of gallstone pancre-
atitis shows a large homogeneous fluid collection in the
lesser sac (*) with no nonliquefied components and a
thick enhancing wall (arrows), findings that are consis-
tent with pseudocyst.
2 weeks better shows the internal heterogeneity
of an ANC (2).
If an APFC has not resolved after 4 weeks, it
becomes more organized and develops a capsule
that manifests as an enhancing wall at contrast-
enhanced CT. At this point, the collection is
referred to as a pseudocyst (Fig 5), and, since
there is no necrosis, it should contain only fluid
with no nonliquefied components. If there is even
a small area of fat or soft-tissue attenuation in an
otherwise fluid-attenuation collection, the diag-
nosis is not pseudocyst but WON. At MR imag-
ing, pseudocysts are uniformly hyperintense on
T2-weighted images, with no solid components
or debris in the fluid (Fig 6). Pseudocysts may
have a connection to the pancreatic ductal sys-
tem, which is best seen at MR cholangiopancrea-
tography owing to superior contrast resolution
(Fig 7) (2).These ductal connections can seal off,
often leading to cyst resolution. Pseudocysts de-
velop in fewer than 10% of cases of IEP (16). A
pseudocyst is typically peripancreatic in location,
although it can, on rare occasions, be intrapan-
creatic in cases of prior necrosectomy with a
persistent pancreatic duct leak into the necrosec-
tomy bed. In such cases, a pseudocyst forms be-
cause of disconnected duct syndrome, whereby a
viable pancreatic tail remains after necrosectomy
or pancreatic body necrosis, with the pseudocyst
forming as a result pancreatic juice leakage from
the disconnected duct (Fig 7) (2,17).
ANC and WON
ANCs are present within the first 4 weeks of
symptom onset and are poorly organized necrotic
collections that occur only in necrotizing pancre-
atitis. ANCs are often found in the lesser sac and
pararenal spaces and may extend into the pancreas
within areas of parenchymal necrosis.They are
often multiple, with a loculated appearance, and
may extend inferiorly as far as the pelvic sidewalls.
ANCs typically demonstrate a variable amount
of fluid and can be distinguished from APFCs
by the presence of nonliquefied debris, such as
solid-appearing components or fat globules within
the fluid (Figs 3, 4, 8).When intravenous contrast
material is contraindicated (eg, in a patient with
acute renal failure), the presence of fat attenuation
within a collection at nonenhanced CT is help-
ful for identifying necrosis and diagnosing ANCs
(Fig 9). In the early phase of pancreatitis, differ-
entiating between an APFC and an ANC can be
682  May-June 2016	 radiographics.rsna.org
difficult, and the diagnosis of necrosis may be un-
certain. Imaging in the 2nd week is usually helpful
for distinguishing an APFC from an ANC. Any
peripancreatic collection associated with known
pancreatic parenchymal necrosis should be termed
an ANC, even if it is homogeneous and contains
no nonliquefied debris (2).
After 4 weeks, an ANC typically develops a
thick mature wall, at which point the collection
is referred to as WON. Like pseudocysts, a WON
contains fluid and has a thick enhancing wall.
Unlike pseudocysts, however,WON contains
necrotic fat and/or pancreatic tissue, which are
well demonstrated at both contrast-enhanced CT
and MR imaging as nonliquefied debris within
the fluid (Figs 3c, 10).WON may be confined to
the pancreatic parenchyma but more commonly
occurs in the peripancreatic space and can often
Figure 8.  Infected WON on contrast-enhanced
coronal CT scans in a 25-year-old man with idio-
pathic pancreatitis. (a) On day 7 after symptom
onset, extensive bilateral ANCs are visible in the
pararenal spaces. The ANCs extend to the pelvis (*),
demonstrate heterogeneous fluid attenuation, and
contain nonliquefied debris, including fat globules
(arrows). (b) On day 15, the collection (*) has a
more organized appearance, and it is easier to iden-
tify necrotic fat in the collection (arrow). (c) On day
42 image obtained after readmission for sepsis, or-
ganized, heterogeneous, gas-containing collections
with thick enhancing walls are present in the parare-
nal space (arrows), findings that are consistent with
infected WON.
Figure 9.  ANC in a 41-year-old woman with
acute pancreatitis. Nonenhanced CT image
obtained 9 days after symptom onset shows
poor contrast resolution between pancreas
and peripancreatic collections, such that ne-
crosis in the pancreas is uncertain. However,
the presence of small fat globules (arrows) in
the peripancreatic collections and the overall
heterogeneity are consistent with necrotizing
pancreatitis with an ANC.
RG  •  Volume 36  Number 3	 Foster et al  683
Figure 10.  Evolution of necrotizing pancreatitis during 2 months in a 48-year-old woman. (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 nonenhanced T2-weighted MR image better shows the
contents of the ANC (*), including hyperintense fluid and nonliquefied 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 (*). (e) Week 6: Endoscopic image from
the gastric body, obtained during cystogastrostomy and debridement, shows necrotic debris (arrow) from the WON.
(f) Week 7: Postprocedure axial contrast-enhanced CT image shows successful decompression of the WON. Multiple
double-pigtail stents traversing the cystogastrostomy (arrows) can be seen.
occur in both locations, with a coalescent collec-
tion extending from the lesser sac into a portion
of parenchyma (Fig 10) (2).There is evidence
that MR imaging outperforms CT, with higher
interreader agreement, in the assessment of the
ratio of fluid to necrotic debris in collections
older than 4 weeks.Therefore, MR imaging is a
valuable alternative to contrast-enhanced CT for
planning interventions because it allows determi-
nation of the amount of necrotic debris that must
be removed by means of more aggressive inter-
ventions (Fig 11) (18).
684  May-June 2016	 radiographics.rsna.org
Figure 11.  Necrotizing pancreatitis in a 47-year-old man in week 16 of persistent symptoms. (a) Axial
nonenhanced CT image shows pancreatic WON involving nearly the entire pancreas (arrows); at least
half of its volume appears to contain fluid. (b) Subsequent axial fat-saturated T2-weighted MR image
shows the WON (arrows) containing mostly nonliquefied debris and pancreatic necrosis, with little fluid
present. Such a collection would respond poorly to percutaneous or endoscopic drainage and would
require more aggressive therapy.
Infection
and Local Complications
Any collection can be sterile or infected, although
infection occurs far more frequently in necrotic
collections (2). Clinically, infection is suspected
in a previously stable patient who experiences
decompensation with signs of infection (19).
The only imaging finding of an infected collec-
tion 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 collec-
tion owing to the complex nature of necrotic
collections (Figs 8, 12) (2). Infected collections
can also manifest with gas bubbles due to a
pancreatic-enteric fistula, which can occasionally
be seen when necrotic collections erode through
the bowel wall, most commonly in the colon and
duodenum (Fig 13) (20). In one series, an enteric
fistula occurred in 4% of patients hospitalized for
acute pancreatitis (21). Gas within the pancre-
atic duct can also mimic gas within a pancreatic
collection but generally has an identifiable linear
distribution and typically occurs in the clinical
context of recent endoscopic pancreatography or
pancreatic duct stent placement (Fig 14).
The use of imaging-guided fluid collection
aspiration or necrotic tissue fine-needle aspira-
tion to help diagnose infection prior to invasive
therapeutic necrosectomy has both advantages
and disadvantages, and the topic is still widely
debated. At some institutions, fine-needle aspira-
tion has fallen out of favor in recent years, partly
due to a shift in preference toward early conser-
vative management with percutaneous drainage,
which may delay or even obviate surgical inter-
vention. If percutaneous drainage is performed,
culture of the fluid can be performed at the same
time (19,22). Another argument against fine-
needle aspiration is that one must consider the
substantial false-negative (sampling too early)
and false-positive (contamination) results of the
procedure (25% and 15%, respectively). At some
institutions, fine-needle aspiration is thought to
be helpful when clinical signs and imaging find-
ings are confusing or complicated and the ben-
efits of diagnosis of infection outweigh the risk of
iatrogenic introduction of infection (22).
In addition to infection, vascular complica-
tions are common, occurring in a quarter of
patients with acute pancreatitis, and can cause
substantial morbidity and mortality.Two separate
pathophysiologic processes lead to vascular com-
plications. First, inflammatory reactions can lead
to splenic vein thrombosis, the most common
vascular complication (23). Second, pancreatic
enzymes can cause vessel erosion and lead to ei-
ther spontaneous arterial hemorrhage or pseu-
doaneurysm of (in order of decreasing frequency)
the splenic, gastroduodenal, and pancreaticoduo-
denal arteries (24). A detailed discussion of these
complications is beyond the scope of this article,
as their evaluation is not specified under the
revised Atlanta classification.We direct the reader
to other excellent publications that describe these
complications (25).
RG  •  Volume 36  Number 3	 Foster et al  685
Figure 14.  Necrotizing pancreatitis at week 3 in a
59-year-old man. Axial contrast-enhanced CT image
obtained 3 weeks after disease onset shows necrosis of
pancreatic neck, body, and tail (*), as well as peripan-
creatic necrosis. A small focus of gas (white arrow) in
the pancreatic duct in the necrotic pancreatic body is
secondary to recent stent placement in the duct (black
arrow) and thus does not represent an infected ANC.
Figure 13.  Necrotizing pancreatitis in a 74-year-old
woman. Axial contrast-enhanced CT image obtained at
5 weeks shows peripancreatic WON with multiple foci
of gas (*). A large fistula is seen to the distal transverse
colon and contains gas and fluid (arrows), a finding that
explains the development of gas in the WON.
Figure 12.  Necrotizing pancreatitis in a 37-year-old woman. (a) Axial contrast-enhanced CT image obtained
in week 3 shows the pancreatic tail (*) and a peripancreatic ANC containing nonliquefied debris with foci of
fat attenuation (arrows). (b) Axial contrast-enhanced CT image obtained in week 6 because the patient experi-
enced decompensation and was readmitted shows organization of the collection (*) with multiple new foci of
gas, findings that are consistent with infected WON.
Management Implications
Various interventions are available for managing
local complications of acute pancreatitis, with a
range of invasiveness and, therefore, morbidity;
these include percutaneous drainage, endoscopic
cystogastrostomy, endoscopic débridement (Fig
10), and surgical necrosectomy (19). Newer ap-
proaches have focused on a combined “step-up”
approach in which percutaneous drainage cath-
eters are placed in necrotic collections, followed
by minimally invasive débridements along the
catheter tract if the patient fails to improve within
72 hours (26). Although these minimally invasive
techniques have been replacing open surgical
débridement, the previous standard of care, more
recent studies in which open necrosectomy has
been reanalyzed have found low mortality rates
and results comparable to those achieved with
minimally invasive techniques (27).While exact
treatment regimens vary among institutions,
collections generally do not warrant intervention
unless there are persistent symptoms, inability
to maintain nutrition, or signs of infection (28).
By implementing the revised Atlanta classifica-
tion, the radiologist is able to help the care team
prescribe the appropriate therapy according to
the type of collection. For instance, in the case of
a lesser sac pseudocyst necessitating drainage, the
gastroenterologist may create a cystogastrostomy
with the use of endoscopic US, a procedure with
686  May-June 2016	 radiographics.rsna.org
a high success rate (29). However, if the collec-
tion represents WON, adequate drainage may
not be achieved with this approach owing to the
nonliquefied components and, therefore, neces-
sitating more aggressive débridement through the
endoscope as a first-line therapy (Fig 11).
Suggestions for Reporting
When reviewing a patient’s history, it is important
to note the time elapsed since the 1st day of ab-
dominal pain, as this defines the time course used
to stratify local complications. A statement about
the presence or absence of necrosis should be
made, and the location (peripancreatic, pancreatic,
or both) and amount of necrotic gland (<30% or
>30%) should be documented. Local complica-
tions should be described in terms of location
(lesser sac, anterior pararenal space, transverse
mesocolon, etc), size, appearance, and presence or
absence of a mature wall. Specifically, the contents
of local complications should be described either
as homogeneous with fluid attenuation (APFC
or pseudocyst) or as having nonliquefied necrotic
components (ANC orWON). Finally, the col-
lection should be specifically named according
to the revised Atlanta classification lexicon, with
the subtype of pancreatitis and the number of
weeks since the onset of abdominal pain (<4 or
≥4 weeks) taken into account (Fig 15).We sug-
gest that the findings be succinctly summarized
in the impression section of the report (eg, IEP or
necrotizing pancreatitis with type and location of
collection) and a statement that the revised Atlanta
classification was used so that multidisciplinary
team members recognize the expertise and the
standardization of terminology.
Conclusion
Incorporation of the revised Atlanta classification
system into everyday practice updates and stan-
dardizes terminology, which facilitates accurate
documentation of the range of imaging findings
in acute pancreatitis. It is important to remember
that pancreatitis-related collections are not always
fluid filled, and evaluation for nonliquefied compo-
nents is essential for differentiating collections that
contain only fluid (APFCs and pseudocysts) from
those that contain necrotic nonliquefied debris
(ANCs andWON). In general, imaging findings
combined with the time course of the disease allow
clear differentiation between the collections and en-
able stratification among different treatment plans,
facilitating the radiologist’s seamless integration
into a multidisciplinary team of gastroenterologists,
intensivists, interventionalists, and surgeons.
References
	 1.	Bradley EL 3rd. A clinically based classification system for
acute pancreatitis: summary of the International Symposium
on Acute Pancreatitis, Atlanta, Ga, September 11–13, 1992.
Arch Surg 1993;128(5):586–590.
	 2.	Banks PA, Bollen TL, Dervenis C, et al. Classification of
acute pancreatitis 2012: revision of the Atlanta classification
and definitions by international consensus. Gut 2013;62(1):
102–111.
	 3.	The Pancreas Club, Inc. Revision of the Atlanta classifica-
tion of acute pancreatitis. Available at: http://pancreasclub
.com/wp-content/uploads/2011/11/AtlantaClassification.pdf.
Published April 9, 2008. Accessed March 28, 2015.
	 4.	Thoeni RF. The revised Atlanta classification of acute pan-
creatitis: its importance for the radiologist and its effect on
treatment. Radiology 2012;262(3):751–764.
	 5.	 BollenTL.Imagingofacutepancreatitis:updateoftherevised
Atlanta classification. Radiol Clin North Am 2012;50(3):
429–445.
	 6.	 Sheu Y, Furlan A, Almusa O, Papachristou G, Bae KT. The
revisedAtlantaclassificationforacutepancreatitis:aCTimag-
ingguideforradiologists.EmergRadiol2012;19(3):237–243.
Figure 15.  Decision tree for re-
porting according to the revised
Atlanta classification.
RG  •  Volume 36  Number 3	 Foster et al  687
	 7.	 Bollen TL, Besselink MG, van Santvoort HC, Gooszen HG,
van Leeuwen MS. Toward an update of the Atlanta classifi-
cation on acute pancreatitis: review of new and abandoned
terms. Pancreas 2007;35(2):107–113.
	 8.	 DunnickNR,LanglotzCP.Theradiologyreportofthefuture:
a summary of the 2007 Intersociety Conference. J Am Coll
Radiol 2008;5(5):626–629.
	 9.	 Ellenbogen PH. BI-RADS: revised and replicated. J Am Coll
Radiol 2014;11(1):2.
10.		Yadav D, Lowenfels AB. The epidemiology of pancreatitis
and pancreatic cancer. Gastroenterology 2013;144(6):
1252–1261.
11.		Petrov MS, Windsor JA. Classification of the severity of
acute pancreatitis: how many categories make sense? Am J
Gastroenterol 2010;105(1):74–76.
12.		 Baker ME, Nelson RC, Rosen MP, et al. ACR Appropriate-
ness Criteria acute pancreatitis. Ultrasound Q 2014;30(4):
267–273.
13.		Singh VK, Bollen TL, Wu BU, et al. An assessment of the
severityofinterstitialpancreatitis.ClinGastroenterolHepatol
2011;9(12):1098–1103.
14.		Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung
CL, Sibbald WJ. Multiple organ dysfunction score: a reliable
descriptor of a complex clinical outcome. Crit Care Med
1995;23(10):1638–1652.
15.		Spanier BW, Nio Y, van der Hulst RW, Tuynman HA,
Dijkgraaf MG, Bruno MJ. Practice and yield of early CT
scan in acute pancreatitis: a Dutch observational multicenter
study. Pancreatology 2010;10(2-3):222–228.
16.		 Lenhart DK, Balthazar EJ. MDCT of acute mild (nonnecro-
tizing)pancreatitis:abdominalcomplicationsandfateoffluid
collections. AJR Am J Roentgenol 2008;190(3):643–649.
17.		Sandrasegaran K, Tann M, Jennings SG, et al. Disconnec-
tion of the pancreatic duct: an important but overlooked
complication of severe acute pancreatitis. RadioGraphics
2007;27(5):1389–1400.
18.		Kamal A, Singh VK, Akshintala VS, et al. CT and MRI
assessmentofsymptomaticorganizedpancreaticfluidcollec-
tionsandpancreaticductdisruption:aninterreadervariability
study using the revised Atlanta classification 2012. Abdom
Imaging 2015;40(6):1608–1616.
19.		 FreemanML,WernerJ,vanSantvoortHC,etal.Interventions
for necrotizing pancreatitis: summary of a multidisciplinary
consensus conference. Pancreas 2012;41(8):1176–1194.
20.		Tüney D, Altun E, Barlas A, Yegen C. Pancreatico-colonic
fistula after acute necrotizing pancreatitis: diagnosis with
spiral CT using rectal water soluble contrast media. JOP
2008;9(1):26–29.
21.		Kochhar R, Jain K, Gupta V, et al. Fistulization in the GI
tract in acute pancreatitis. Gastrointest Endosc 2012;75(2):
436–440.
22.		 vanBaalMC,BollenTL,BakkerOJ,etal.Theroleofroutine
fine-needle aspiration in the diagnosis of infected necrotizing
pancreatitis. Surgery 2014;155(3):442–448.
23.		Türkvatan A, Erden A, Türkoğlu MA, Seçil M, Yüce G.
Imaging of acute pancreatitis and its complications. II.
Complications of acute pancreatitis. Diagn Interv Imaging
2015;96(2):161–169.
24.		 Memiş A, Parildar M. Interventional radiological treatment
in complications of pancreatitis. Eur J Radiol 2002;43(3):
219–228.
25.		Shyu JY, Sainani NI, Sahni VA, et al. Necrotizing pancre-
atitis: diagnosis, imaging, and intervention. RadioGraphics
2014;34(5):1218–1239.
26.		 vanSantvoortHC,BesselinkMG,BakkerOJ,etal.Astep-up
approach or open necrosectomy for necrotizing pancreatitis.
N Engl J Med 2010;362(16):1491–1502.
27.		 MadenciAL,MichailidouM,ChiouG,ThabetA,Fernández-
delCastilloC,FagenholzPJ.Acontemporaryseriesofpatients
undergoing open debridement for necrotizing pancreatitis.
Am J Surg 2014;208(3):324–331.
28.		 WuBU,BanksPA.Clinicalmanagementofpatientswithacute
pancreatitis. Gastroenterology 2013;144(6):1272–1281.
29.		Varadarajulu S, Christein JD, Tamhane A, Drelichman
ER, Wilcox CM. Prospective randomized trial compar-
ing EUS and EGD for transmural drainage of pancreatic
pseudocysts(withvideos).GastrointestEndosc2008;68(6):
1102–1111.
This journal-based SA-CME activity has been approved for AMA PRA Category 1 Credit
TM
. See www.rsna.org/education/search/RG
1
Errata
ERRATA
May-June 2019 • Volume 39 • Number 3
Originally published in:
RadioGraphics 2018; 38 (6):1609-1616 • https://
doi.org/10.1148/rg.2018180031
Rules and Regulations Relating to Roles of Non-
physician Providers in Radiology Practices
C. Matthew Hawkins
Erratum in:
RadioGraphics 2019:39(3):XXXX • https://doi.
org/10.1148/rg.2019XXXXX
Second paragraph, second column, p 1610: The
sixth sentence should read as follows: “The authors of a
review article emphasized that employing RAs increases
physician supervision in nearly all clinical settings and
that billing for services provided by RAs without ap-
propriate supervision violates the False Claims Act.”
Originally published in:
RadioGraphics 2018; 32(2):1421–1440 • https://doi.
org/10.1148/rg.2018180041
Radiation Dose Reduction at Pediatric CT: Use of
Low Tube Voltage and Iterative Reconstruction
Yasunori Nagayama, Seitaro Oda,Takeshi Nakaura,
Akinori Tsuji, Joji Urata, Mitsuhiro Furusawa,
Daisuke Utsunomiya,Yoshinori Funama, Masafumi
Kidoh,YasuyukiYamashita
Erratum in:
RadioGraphics 2019:39(3):XXXX • https://doi.
org/10.1148/rg.2019XXXXX
First sentence, third full paragraph, p 1425: The
sentence should read as follows: “Radiation output is
proportional to the square of tube voltage but shows a
linear relationship with tube current.”
Originally published in:
RadioGraphics 2016; 36(3):675–687 • https://doi.
org/10.1148/rg.2016150097
Revised Atlanta Classification for Acute Pancreatitis:
A Pictorial Essay
Bryan R. Foster, Kyle K. Jensen, Gene Bakis, Akram
M. Shaaban, Fergus V. Coakley
Erratum in:
RadioGraphics 2019:39(3):XXXX • https://doi.
org/10.1148/rg.2019XXXXX
Note,Table 1: The abbreviation for IEP should read as
follows: “IEP = interstitial edematous pancreatitis.”
Originally published in:
RadioGraphics 2012; 32(2):437–451 • https://doi.
org/10.1148/rg.322115032
Peritoneal and Retroperitoneal Anatomy and Its
Relevance for CrossSectional Imaging
Temel Tirkes, Kumaresan Sandrasegaran, Aashish
A. Patel, Margaret A. Hollar, Juan G. Tejada, Mark
Tann, Fatih M. Akisik, John C. Lappas
Erratum in:
RadioGraphics 2019:39(3):XXXX • https://doi.
org/10.1148/rg.2019XXXXX
First sentence, p 447: The first sentence should read
as follows: “The retroperitoneum is divided into three
distinct compartments: the posterior pararenal space,
bounded by the transversalis fascia posteriorly; the
anterior pararenal space, bounded by the parietal peri-
toneum anteriorly; and the perirenal space, bounded
by the perirenal fascia (Fig 12a, 12b).”

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pancreas 3.pdf

  • 1. GASTROINTESTINAL IMAGING 675 Revised Atlanta Classification for Acute Pancreatitis: A Pictorial Essay1 The 2012 revised Atlanta classification is an update of the original 1992 Atlanta classification, a standardized clinical and radiologic nomenclature for acute pancreatitis and associated complications based on research advances made over the past 2 decades. Acute pancreatitis is now divided into two distinct subtypes, necrotizing pancreatitis and interstitial edematous pancreatitis (IEP), based on the presence or absence of necrosis, respectively.The revised clas- sification system also updates confusing and sometimes inaccurate terminology that was previously used to describe pancreatic and peripancreatic collections. As such, use of the terms acute pseudo- cyst and pancreatic abscess is now discouraged. Instead, four distinct collection subtypes are identified on the basis of the presence of pancreatic necrosis and time elapsed since the onset of pancreatitis. Acute peripancreatic fluid collections (APFCs) and pseudocysts occur in IEP and contain fluid only. Acute necrotic collections (ANCs) and walled-off necrosis (WON) occur only in patients with necrotizing pancreatitis and contain variable amounts of fluid and necrotic debris. APFCs and ANCs occur within 4 weeks of disease onset. After this time, APFCs or ANCs may either resolve or per- sist, developing a mature wall to become a pseudocyst or aWON, respectively. Any collection subtype may become infected and man- ifest as internal gas, though this occurs most commonly in necrotic collections. In this review, the authors present a practical image-rich guide to the revised Atlanta classification system, with the goal of fostering implementation of the revised system into radiology prac- tice, thereby facilitating accurate communication among clinicians and reinforcing the radiologist’s role as a key member of a multidis- ciplinary team in treating patients with acute pancreatitis. © RSNA, 2016 • radiographics.rsna.org Bryan R. Foster, MD Kyle K. Jensen, MD Gene Bakis, MD Akram M. Shaaban, MBBCh FergusV . Coakley, MD Abbreviations: ANC = acute necrotic collec- tion, APFC = acute peripancreatic fluid collec- tion, IEP = interstitial edematous pancreatitis, WON = walled-off necrosis RadioGraphics 2016; 36:675–687 Published online 10.1148/rg.2016150097 Content Codes: 1 From the Department of Diagnostic Radiol- ogy, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239 (B.R.F., K.K.J., G.B., F.V.C.); and Department of Radiology, University of Utah, Salt Lake City, Utah (A.M.S.). Presented as an education ex- hibit at the 2014 RSNA Annual Meeting. Re- ceived April 6, 2015; revision requested June 30 and received August 10; accepted August 31. For this journal-based SA-CME activity, the authors, editor, and reviewers have disclosed no relevant relationships. Address correspondence to B.R.F. (e-mail: fosterbr@ohsu.edu). © RSNA, 2016 After completing this journal-based SA-CME activity, participants will be able to: ■ Discuss the revised Atlanta classifica- tion system. ■ Distinguish interstitial edematous pan- creatitis from necrotizing pancreatitis at imaging. ■ Describe the imaging appearance of pancreatitis-associated collections, in- cluding acute peripancreatic fluid collec- tions, pseudocysts, acute necrotic collec- tions, and walled-off necrosis. See www.rsna.org/education/search/RG. SA-CME LEARNING OBJECTIVES Introduction Beginning in 2007, the Acute Pancreatitis Classification Working Group polled an international cohort of pancreatic experts, includ- ing 11 pancreatic societies, with the goal of revising the original 1992 Atlanta classification system for acute pancreatitis (1,2). Although the original Atlanta classification system established common terms for acute pancreatitis and related complications, the nomenclature proved to be confusing, leading to incorrect use of terms in both clinical practice and research. In addition, advances in imaging and in the understanding of pathophysiology necessitated substantial revision of the classification system (2). A draft was posted on the Pancreas Club Web site in 2008 (3).This draft was referrenced in several initial publications in the radiology literature (4–6). After a total of four Web-based revisions, the revised Atlanta classification system was finalized in 2012 and published shortly thereafter, with updates to the earlier-cited draft (2). An earlier incorrect version of this article appeared online. This article was corrected on March 28, 2019. This copy is for personal use only. To order printed copies, contact reprints@rsna.org
  • 2. 676  May-June 2016 radiographics.rsna.org recognized by the working group that previously used terms such as acute pseudocyst and pancreatic abscess were confusing and had fallen out of favor, in addition to their not being entirely descriptive of the pathologic condition.Therefore, a specific lexicon was needed to distinguish necrotic from nonnecrotic collections (7). Use of standardized reporting schemas and application of a well- defined lexicon to a specific disease are thought to be important for effective communication and quality care and are in fact becoming more common in everyday radiologic practice (8,9). Most important, adoption of such standardized terminology allows the radiologist to be an effec- tive member of a multidisciplinary team in the diagnosis and treatment of acute pancreatitis. The purpose of this article is to serve as an im- age-rich practical overview of the revised Atlanta classification system such that the radiologist will have a working understanding of the system and can immediately incorporate the lexicon into clinical practice.To that end, we focus on key imaging characteristics that help differenti- ate collections that often have a similar appear- ance, describe various infectious complications, and discuss imaging pitfalls. In addition, we will propose a reporting schema to facilitate accurate communication. Acute Pancreatitis: Over- view and New Diagnostic Criteria Acute pancreatitis is an acute inflammatory condition, with a range of severity as well as vari- ous local and systemic complications. Gallstones and alcohol are the first and second most com- mon causes of acute pancreatitis, respectively, and additional variants occur when patients are stratified by sex. In 2009, acute pancreatitis was the most common cause of hospital admission for gastrointestinal disorders in the United States, with approximately 275 000 admissions, nearly double the number in the previous decade.This increase is thought to be secondary not only to nationwide increases in obesity and the incidence of gallstones, but also to more sensitive and more frequently used laboratory testing (10). A majority of patients have mild acute pancreatitis, which car- ries essentially no risk of mortality. In the subset of patients with organ failure (severe disease) or in- fected necrosis, however, the mortality rate reaches 30% (2,11).The revised Atlanta classification requires that two or more of the following crite- ria be met for the diagnosis of acute pancreatitis: (a) abdominal pain suggestive of pancreatitis, (b) serum amylase or lipase level greater than three times the upper normal value, or (c) characteristic imaging findings (2). Contrast material–enhanced CT is most commonly used to fulfill the radiologic One major component of the revised classifi- cation system that is of particular importance to radiologists is the manner in which pancreatitis- associated collections (local complications) are described and named (Table 1). It was well TEACHING POINTS ■ ■ In the 1st week after the onset of pancreatitis, imaging findings correlate poorly with clinical severity, and imaging sensitivity for necrotizing pancreatitis is decreased in the first few days. In addition, any local complications that are detected in the 1st week generally do not necessitate intervention because treat- ment is based on supportive measures and management of or- gan failure. Initial imaging is most useful when performed 5–7 days after hospital admission, when local complications have developed and pancreatic necrosis (if present) should be clearly distinguishable. ■ ■ In the revised classification system, new definitions were cre- ated to clearly stratify acute pancreatitis into two subcategories based on imaging findings: IEP and necrotizing pancreatitis. IEP is more common and represents nonnecrotizing inflam- mation of the pancreas. The entire pancreas will enhance at contrast-enhanced CT or MR imaging, with no unenhanced (necrotic) areas, although enhancement of the gland may be less avid than that of the normal pancreas owing to interstitial edema. IEP usually manifests with focal or diffuse pancreatic enlargement and is typically surrounded by wispy peripancre- atic inflammation or a small amount of fluid. In addition, there should be no surrounding peripancreatic necrotic collections in IEP, although there may be surrounding fluid-containing collections. Necrotizing pancreatitis accounts for 5%–10% of cases of acute pancreatitis. It is important to understand that necrosis may involve either the pancreatic parenchyma or the peripancreatic tissues and in both cases is termed necrotizing pancreatitis. There are three subtypes of necrotizing pancreati- tis; the subtypes are based on the anatomic area of necrotic involvement: (a) pancreatic only, (b) peripancreatic only, and (c) combined pancreatic and peripancreatic. ■ ■ The revised Atlanta classification makes an important distinc- tion between collections that contain purely fluid (those en- countered in nonnecrotizing pancreatitis and IEP) and collec- tions that contain necrotic debris in addition to fluid (those encountered in necrotizing pancreatitis). The terms acute pseudocyst and pancreatic abscess have been abandoned. Similarly, the use of the term pseudocyst in radiology reporting to describe any pancreatitis-related collection is misleading to treating physicians, since the term implies that these collections always contain purely fluid, which is not the case in necrotic collections. Instead, the revised classification includes new defi- nitions that more accurately describe the various types of col- lections encountered: APFC, pseudocyst, ANC, and WON. The important distinctions for classifying collections correctly are the time course (≤4 weeks or >4 weeks from onset of pain) and the presence or absence of necrosis at imaging. ■ ■ If an APFC has not resolved within 4 weeks, it becomes more organized, with development of a capsule that manifests as an enhancing wall at contrast-enhanced CT. At this point, the collection is referred to as a pseudocyst, and, since there is no necrosis, it should contain only fluid with no nonliquefied com- ponents. If there is even a small area of fat or soft-tissue attenu- ation in an otherwise fluid-attenuation collection, the diagnosis is not pseudocyst but WON. ■ ■ Any collection can be sterile or infected, although infection oc- curs far more frequently in necrotic collections. Clinically, infec- tion 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).
  • 3. RG  •  Volume 36  Number 3 Foster et al  677 patients as having either severe or mild pancreati- tis on the basis of the presence or absence of or- gan failure, respectively (1). However, emerging evidence indicated that a large subset of patients with local complications experienced substantial morbidity but little mortality (11).Therefore, a third category was added to the new classifica- tion—moderately severe acute pancreatitis—to describe this patient group (2). Organ failure and local complications are not seen in patients with mild pancreatitis, who are usually discharged within the 1st week, with very low mortality (13).These patients rarely require CT for local complications, and imaging may be useful only in assessing the cause of pancreatitis (eg, ultraso- nography [US] or MR cholangiopancreatography for choledocholithiasis) (12). Moderately severe acute pancreatitis manifests in patients with transient organ failure lasting less than 48 hours and/or local or systemic complica- tions. Systemic complications are generally co- morbidities exacerbated by pancreatitis, such as acute kidney injury in the setting of chronic renal failure. Local complications include a variety of pancreatic and peripancreatic collections. Such collections generally develop in the 2nd week (the late phase of pancreatitis) and are clinically suspected in patients with unremitting or recur- rent pain, a secondary peak in pancreatic enzyme levels, worsening organ dysfunction, or sepsis (2).These symptoms should prompt imaging studies such as (in order of preference) contrast- enhanced CT, contrast-enhanced MR imaging, or unenhanced MR imaging (12). Severe disease is characterized by organ failure that persists for more than 48 hours. Because criterion, but magnetic resonance (MR) imaging is also appropriate. Although many patients will meet the criteria for acute pancreatitis on the basis of symptoms and laboratory results alone and may not require imaging initially, imaging may be per- formed early in the disease course when the cause of the disease is unclear, to look for causative factors such as choledocholithiasis and pancreatic cancer. Imaging for the diagnosis of pancreatitis is also appropriate when abdominal pain suggests pancreatitis but the amylase or lipase level is not elevated to the threshold value, which is often the case at delayed presentation (12).The onset of pancreatitis is considered to coincide with the 1st day of pain, not the day on which the patient pres- ents for care or the day of hospital admission (2). Phases of Acute Pancreatitis In pathophysiologic terms, acute pancreatitis is divided into early and late phases.The early phase occurs in the 1st week after onset, with the disease manifesting as a systemic inflammatory response. At this time, clinical severity and treatment are mainly determined on the basis of type and degree of organ failure.The late phase, which generally starts in the 2nd week and can last for weeks to months, occurs only in patients with moderately severe or severe pancreatitis, as defined by persis- tent organ failure and by local complications (2). Grading of Severity of Acute Pancreatitis To improve the stratification of patients at the time of presentation, the pancreatitis severity scale was updated in the revised Atlanta clas- sification.The original classification categorized Table 1: Pancreatic and Peripancreatic Collections Collection Time after Onset of Pain (wk) Pancreatitis Subcategory Location Imaging Features APFC 4 IEP Extrapancreatic Homogeneous, fluid attenuation, con- forms to retroperitoneal structures, no wall ANC 4 Necrotizing pancreatitis Intra- and/or extra- pancreatic Inhomogeneous*, nonliquefied com- ponents†, no wall Pseudocyst >4 IEP Extrapancreatic‡ Homogeneous, fluid filled, circum- scribed, encapsulated with wall WON >4 Necrotizing pancreatitis Intra- and/or extra- pancreatic Inhomogeneous, nonliquefied compo- nents, encapsulated with wall Sources.—References 2–4. Note.—Any collection may become infected. ANC = acute necrotic collection, APFC = acute peripancreatic fluid collection, IEP = interstitial edematous pancreatitis, WON = walled-off necrosis. *Early ANCs may be homogeneous; follow-up computed tomography (CT) performed in 2nd week may help clarify status. †Includes solid-appearing components or fat globules within fluid. ‡Rarely, persistent pancreatic leak or disconnected duct may lead to intrapancreatic pseudocyst.
  • 4. 678  May-June 2016 radiographics.rsna.org organ failure plays a key role in determining disease severity, an accurate definition is essential for clinical management of acute pancreatitis. The modified Marshall scoring system (Table 2) is endorsed in the revised Atlanta classification as the primary method for determining organ failure.The modified Marshall scoring system incorporates measurements from the respiratory, cardiovascular, and renal systems, with a score of 2 or higher for any system indicating organ failure (2,14). In the 1st week after the onset of pancreatitis, imaging findings correlate poorly with clinical severity, and imaging sensitivity for necrotizing pancreatitis is decreased in the first few days (2). In addition, any local complications detected in the 1st week generally do not neces- sitate intervention because treatment is based on supportive measures and management of organ failure (15). Initial imaging is most useful when performed 5–7 days after hospital admission, when local complications have developed and pancreatic necrosis (if present) should be clearly distinguishable (2). IEP versus Necrotizing Pancreatitis In the revised classification system, new defini- tions were created to clearly stratify acute pan- creatitis into two subcategories based on imaging findings: IEP and necrotizing pancreatitis. IEP is more common and represents nonnecrotiz- ing inflammation of the pancreas.The entire pancreas will enhance at contrast-enhanced CT or MR imaging, with no unenhanced (necrotic) areas, although enhancement of the gland may be less avid than that of the normal pancreas owing to interstitial edema. IEP usually manifests with focal or diffuse pancreatic enlargement and is typically surrounded by wispy peripancreatic inflammation or a small amount of fluid (Fig 1). In addition, there should be no surrounding peri- pancreatic necrotic collections in IEP, although there may be surrounding fluid-containing collec- tions (Fig 2). Necrotizing pancreatitis accounts for 5%–10% of cases of acute pancreatitis (2). It is important to understand that necrosis may involve either the pancreatic parenchyma or the peripancreatic tissues and in both cases is termed necrotizing pancreatitis. There are three subtypes of necro- tizing pancreatitis; the subtypes are based on the anatomic area of necrotic involvement: (a) pancreatic only, (b) peripancreatic only, and (c) combined pancreatic and peripancreatic. The latter subtype is the most common, accounting for 75% of cases.The combined subtype dem- onstrates nonenhancing pancreatic parenchyma, as well as nonenhancing heterogeneous peripan- creatic collections, and typically accumulating in the lesser sac and anterior pararenal space (Fig 3a). Peripancreatic necrosis alone, in which the pancreas enhances normally but the peripan- creatic tissues show necrosis, with collections containing variable amounts of fluid and nonliq- Table 2: Modified Marshall Scoring System Organ System Score 0 Score 1 Score 2 Score 3 Score 4 Respiratory* >400 301–400 201–300 101–200 100 Renal: serum creati- nine (mg/dL) 1.4 1.5–1.8 1.9–3.5 3.6–4.9 5 Cardiovascular: sys- tolic blood pressure (mm Hg) >90 <90, responding to fluid resusci- tation <90, not respond- ing to fluid resus- citation <90 with pH <7.3 <90 with pH <7.2 Sources.—References 2,4,14. Note.—A score of 2 or higher indicates organ failure, with transient failure lasting less than 48 hours and persis- tent failure lasting more than 48 hours. *Partial pressure of oxygen/fraction of inspired oxygen, or Pao2 /Fio2 . Figure 1.  IEP in a 28-year-old man with alcohol-related pancreatitis. Axial con- trast-enhanced CT image shows wispy peripancreatic inflammation (arrows) with normal pancreatic enhancement and no collections.
  • 5. RG  •  Volume 36  Number 3 Foster et al  679 uefied components, occurs in 20% of cases (Fig 3b). Pancreatic necrosis alone is the least com- mon subtype, occurring in 5% of cases, and lacks peripancreatic collections (Fig 3c).When imaging is performed within the first few days of disease onset, necrosis may not be detected because the pancreas can appear edematous and globally or focally hypoenhancing and, as such, may be indistinguishable from IEP. In these cases, repeat Figure 2.  IEP in a 43-year-old man. Axial contrast-enhanced CT image shows peripan- creatic inflammation (black arrow) and a homogeneous fluid-attenuation collection in the left anterior pararenal space (white arrow), a finding that is consistent with APFC. Figure 3.  Subtypes of necrotizing pancreatitis on axial contrast-enhanced CT images. (a) Image of combined pancreatic and peripancreatic necrosis in a 58-year-old woman shows nonenhancement of the body (*), normal enhancement of the pancreatic tail (black arrow), and a large ANC in the lesser sac (white arrows). (b) Image of peripancreatic necrosis alone in an 18-year-old man shows a large, complex, heterogeneous peripancreatic collection (arrows) containing both fluid attenuation and nonliquefied components, consistent with an ANC. Note normal enhancement of the pancreatic parenchyma (*), in- dicative of lack of pancreatic parenchymal necrosis. (c) Image of pancreatic necrosis alone in a 33-year- old man shows a large area of encapsulated fat and nonenhancing pancreatic parenchyma (*), defined as WON. Note a very small amount of residual en- hancing parenchyma at the periphery (arrows). contrast-enhanced CT performed 5–7 days later is more accurate for the diagnosis of necrotizing pancreatitis (2). In general, routine contrast- enhanced CT is adequate for diagnosis, and pancreatic protocol multiphase imaging (arterial and portal phase) is typically unnecessary. If renal failure prevents administration of intravenous contrast material, nonenhanced MR imaging is preferred to nonenhanced CT, although limited availability and the difficulty of imaging criti- cally ill patients are significant limitations of MR
  • 6. 680  May-June 2016 radiographics.rsna.org Figure 4.  IEP with APFCs on axial contrast-enhanced CT images in a 49-year-old man. (a) One day after the onset of pain, IEP is seen with a small, homogeneous, fluid-attenuation collection in the left anterior pararenal space (arrow). The pancreas demonstrates normal enhancement. (b–d) At 10 days after onset of pain, multiple homogeneous fluid collections (*) can be seen in the lesser sac (b) and peripancreatic (c) and bilateral anterior pararenal spaces (d), findings consistent with APFCs. Arrow on c = normally enhancing pancreatic tail. imaging, and nonenhanced CT may be easier in practice (12). Pancreatic and Peripancreatic Collections The revised Atlanta classification makes an important distinction between collections that contain purely fluid (those encountered in IEP) and collections that contain necrotic debris in addition to fluid (those encountered in necrotiz- ing pancreatitis).The terms acute pseudocyst and pancreatic abscess have been abandoned. Similarly, the use of the term pseudocyst in radiology report- ing to describe any pancreatitis-related collection is misleading to treating physicians, since the term implies that these collections always contain purely fluid, which is not the case in necrotic collections. Instead, the revised classification includes new definitions that more accurately describe the various types of collections encoun- tered: APFC, pseudocyst, ANC, and WON.The important distinctions for classifying collections correctly are the time course (4 weeks or >4 weeks from onset of pain) and the presence or absence of necrosis at imaging (Table 1) (2). APFC and Pseudocyst APFCs occur during the first 4 weeks and are present only in patients with IEP. Because the pathogenesis involves inflammation without necrosis, APFCs contain only fluid and are visu- alized as homogeneous fluid-attenuation collec- tions that lack a wall and tend to conform to the retroperitoneal spaces (Fig 4). APFCs are always peripancreatic in location. If a similar-appearing collection is seen within the pancreatic paren- chyma, it is by definition an ANC, and the diag- nosis is no longer IEP but necrotizing pancreatitis (2). Most APFCs resolve spontaneously, and drainage should be not be performed because of the risk of infecting an otherwise sterile collec- tion (16). Just as some cases of IEP and necrotiz- ing pancreatitis can be difficult to distinguish at contrast-enhanced CT during the 1st week, it may also be difficult to distinguish between an APFC and an ANC. In general, repeat imaging at
  • 7. RG  •  Volume 36  Number 3 Foster et al  681 Figure 7.  Pseudocyst in a 55-year-old woman with disconnected duct syndrome. Coronal two-dimensional MR cholangiopancreatographic image shows a large bilobed peripancreatic and intrapancreatic pseudocyst (*) that communicates with the pancreatic tail duct (ar- row), which is mildly dilated. Note the disconnection of the tail duct from the ampulla owing to segmental pancreatic body necrosis. Figure 6.  Pseudocyst in a 48-year-old woman. Coro- nal T2-weighted MR image obtained 8 weeks after onset of pancreatitis shows a large homogeneous col- lection in the lesser sac (*) with uniformly hyperintense fluid signal and no necrotic components, findings that are consistent with pseudocyst. Figure 5.  Pseudocyst in a 36-year-old man. Axial CT image obtained 6 weeks after onset of gallstone pancre- atitis shows a large homogeneous fluid collection in the lesser sac (*) with no nonliquefied components and a thick enhancing wall (arrows), findings that are consis- tent with pseudocyst. 2 weeks better shows the internal heterogeneity of an ANC (2). If an APFC has not resolved after 4 weeks, it becomes more organized and develops a capsule that manifests as an enhancing wall at contrast- enhanced CT. At this point, the collection is referred to as a pseudocyst (Fig 5), and, since there is no necrosis, it should contain only fluid with no nonliquefied components. If there is even a small area of fat or soft-tissue attenuation in an otherwise fluid-attenuation collection, the diag- nosis is not pseudocyst but WON. At MR imag- ing, pseudocysts are uniformly hyperintense on T2-weighted images, with no solid components or debris in the fluid (Fig 6). Pseudocysts may have a connection to the pancreatic ductal sys- tem, which is best seen at MR cholangiopancrea- tography owing to superior contrast resolution (Fig 7) (2).These ductal connections can seal off, often leading to cyst resolution. Pseudocysts de- velop in fewer than 10% of cases of IEP (16). A pseudocyst is typically peripancreatic in location, although it can, on rare occasions, be intrapan- creatic in cases of prior necrosectomy with a persistent pancreatic duct leak into the necrosec- tomy bed. In such cases, a pseudocyst forms be- cause of disconnected duct syndrome, whereby a viable pancreatic tail remains after necrosectomy or pancreatic body necrosis, with the pseudocyst forming as a result pancreatic juice leakage from the disconnected duct (Fig 7) (2,17). ANC and WON ANCs are present within the first 4 weeks of symptom onset and are poorly organized necrotic collections that occur only in necrotizing pancre- atitis. ANCs are often found in the lesser sac and pararenal spaces and may extend into the pancreas within areas of parenchymal necrosis.They are often multiple, with a loculated appearance, and may extend inferiorly as far as the pelvic sidewalls. ANCs typically demonstrate a variable amount of fluid and can be distinguished from APFCs by the presence of nonliquefied debris, such as solid-appearing components or fat globules within the fluid (Figs 3, 4, 8).When intravenous contrast material is contraindicated (eg, in a patient with acute renal failure), the presence of fat attenuation within a collection at nonenhanced CT is help- ful for identifying necrosis and diagnosing ANCs (Fig 9). In the early phase of pancreatitis, differ- entiating between an APFC and an ANC can be
  • 8. 682  May-June 2016 radiographics.rsna.org difficult, and the diagnosis of necrosis may be un- certain. Imaging in the 2nd week is usually helpful for distinguishing an APFC from an ANC. Any peripancreatic collection associated with known pancreatic parenchymal necrosis should be termed an ANC, even if it is homogeneous and contains no nonliquefied debris (2). After 4 weeks, an ANC typically develops a thick mature wall, at which point the collection is referred to as WON. Like pseudocysts, a WON contains fluid and has a thick enhancing wall. Unlike pseudocysts, however,WON contains necrotic fat and/or pancreatic tissue, which are well demonstrated at both contrast-enhanced CT and MR imaging as nonliquefied debris within the fluid (Figs 3c, 10).WON may be confined to the pancreatic parenchyma but more commonly occurs in the peripancreatic space and can often Figure 8.  Infected WON on contrast-enhanced coronal CT scans in a 25-year-old man with idio- pathic pancreatitis. (a) On day 7 after symptom onset, extensive bilateral ANCs are visible in the pararenal spaces. The ANCs extend to the pelvis (*), demonstrate heterogeneous fluid attenuation, and contain nonliquefied debris, including fat globules (arrows). (b) On day 15, the collection (*) has a more organized appearance, and it is easier to iden- tify necrotic fat in the collection (arrow). (c) On day 42 image obtained after readmission for sepsis, or- ganized, heterogeneous, gas-containing collections with thick enhancing walls are present in the parare- nal space (arrows), findings that are consistent with infected WON. Figure 9.  ANC in a 41-year-old woman with acute pancreatitis. Nonenhanced CT image obtained 9 days after symptom onset shows poor contrast resolution between pancreas and peripancreatic collections, such that ne- crosis in the pancreas is uncertain. However, the presence of small fat globules (arrows) in the peripancreatic collections and the overall heterogeneity are consistent with necrotizing pancreatitis with an ANC.
  • 9. RG  •  Volume 36  Number 3 Foster et al  683 Figure 10.  Evolution of necrotizing pancreatitis during 2 months in a 48-year-old woman. (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 nonenhanced T2-weighted MR image better shows the contents of the ANC (*), including hyperintense fluid and nonliquefied 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 (*). (e) Week 6: Endoscopic image from the gastric body, obtained during cystogastrostomy and debridement, shows necrotic debris (arrow) from the WON. (f) Week 7: Postprocedure axial contrast-enhanced CT image shows successful decompression of the WON. Multiple double-pigtail stents traversing the cystogastrostomy (arrows) can be seen. occur in both locations, with a coalescent collec- tion extending from the lesser sac into a portion of parenchyma (Fig 10) (2).There is evidence that MR imaging outperforms CT, with higher interreader agreement, in the assessment of the ratio of fluid to necrotic debris in collections older than 4 weeks.Therefore, MR imaging is a valuable alternative to contrast-enhanced CT for planning interventions because it allows determi- nation of the amount of necrotic debris that must be removed by means of more aggressive inter- ventions (Fig 11) (18).
  • 10. 684  May-June 2016 radiographics.rsna.org Figure 11.  Necrotizing pancreatitis in a 47-year-old man in week 16 of persistent symptoms. (a) Axial nonenhanced CT image shows pancreatic WON involving nearly the entire pancreas (arrows); at least half of its volume appears to contain fluid. (b) Subsequent axial fat-saturated T2-weighted MR image shows the WON (arrows) containing mostly nonliquefied debris and pancreatic necrosis, with little fluid present. Such a collection would respond poorly to percutaneous or endoscopic drainage and would require more aggressive therapy. Infection and Local Complications Any collection can be sterile or infected, although infection occurs far more frequently in necrotic collections (2). Clinically, infection is suspected in a previously stable patient who experiences decompensation with signs of infection (19). The only imaging finding of an infected collec- tion 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 collec- tion owing to the complex nature of necrotic collections (Figs 8, 12) (2). Infected collections can also manifest with gas bubbles due to a pancreatic-enteric fistula, which can occasionally be seen when necrotic collections erode through the bowel wall, most commonly in the colon and duodenum (Fig 13) (20). In one series, an enteric fistula occurred in 4% of patients hospitalized for acute pancreatitis (21). Gas within the pancre- atic duct can also mimic gas within a pancreatic collection but generally has an identifiable linear distribution and typically occurs in the clinical context of recent endoscopic pancreatography or pancreatic duct stent placement (Fig 14). The use of imaging-guided fluid collection aspiration or necrotic tissue fine-needle aspira- tion to help diagnose infection prior to invasive therapeutic necrosectomy has both advantages and disadvantages, and the topic is still widely debated. At some institutions, fine-needle aspira- tion has fallen out of favor in recent years, partly due to a shift in preference toward early conser- vative management with percutaneous drainage, which may delay or even obviate surgical inter- vention. If percutaneous drainage is performed, culture of the fluid can be performed at the same time (19,22). Another argument against fine- needle aspiration is that one must consider the substantial false-negative (sampling too early) and false-positive (contamination) results of the procedure (25% and 15%, respectively). At some institutions, fine-needle aspiration is thought to be helpful when clinical signs and imaging find- ings are confusing or complicated and the ben- efits of diagnosis of infection outweigh the risk of iatrogenic introduction of infection (22). In addition to infection, vascular complica- tions are common, occurring in a quarter of patients with acute pancreatitis, and can cause substantial morbidity and mortality.Two separate pathophysiologic processes lead to vascular com- plications. First, inflammatory reactions can lead to splenic vein thrombosis, the most common vascular complication (23). Second, pancreatic enzymes can cause vessel erosion and lead to ei- ther spontaneous arterial hemorrhage or pseu- doaneurysm of (in order of decreasing frequency) the splenic, gastroduodenal, and pancreaticoduo- denal arteries (24). A detailed discussion of these complications is beyond the scope of this article, as their evaluation is not specified under the revised Atlanta classification.We direct the reader to other excellent publications that describe these complications (25).
  • 11. RG  •  Volume 36  Number 3 Foster et al  685 Figure 14.  Necrotizing pancreatitis at week 3 in a 59-year-old man. Axial contrast-enhanced CT image obtained 3 weeks after disease onset shows necrosis of pancreatic neck, body, and tail (*), as well as peripan- creatic necrosis. A small focus of gas (white arrow) in the pancreatic duct in the necrotic pancreatic body is secondary to recent stent placement in the duct (black arrow) and thus does not represent an infected ANC. Figure 13.  Necrotizing pancreatitis in a 74-year-old woman. Axial contrast-enhanced CT image obtained at 5 weeks shows peripancreatic WON with multiple foci of gas (*). A large fistula is seen to the distal transverse colon and contains gas and fluid (arrows), a finding that explains the development of gas in the WON. Figure 12.  Necrotizing pancreatitis in a 37-year-old woman. (a) Axial contrast-enhanced CT image obtained in week 3 shows the pancreatic tail (*) and a peripancreatic ANC containing nonliquefied debris with foci of fat attenuation (arrows). (b) Axial contrast-enhanced CT image obtained in week 6 because the patient experi- enced decompensation and was readmitted shows organization of the collection (*) with multiple new foci of gas, findings that are consistent with infected WON. Management Implications Various interventions are available for managing local complications of acute pancreatitis, with a range of invasiveness and, therefore, morbidity; these include percutaneous drainage, endoscopic cystogastrostomy, endoscopic débridement (Fig 10), and surgical necrosectomy (19). Newer ap- proaches have focused on a combined “step-up” approach in which percutaneous drainage cath- eters are placed in necrotic collections, followed by minimally invasive débridements along the catheter tract if the patient fails to improve within 72 hours (26). Although these minimally invasive techniques have been replacing open surgical débridement, the previous standard of care, more recent studies in which open necrosectomy has been reanalyzed have found low mortality rates and results comparable to those achieved with minimally invasive techniques (27).While exact treatment regimens vary among institutions, collections generally do not warrant intervention unless there are persistent symptoms, inability to maintain nutrition, or signs of infection (28). By implementing the revised Atlanta classifica- tion, the radiologist is able to help the care team prescribe the appropriate therapy according to the type of collection. For instance, in the case of a lesser sac pseudocyst necessitating drainage, the gastroenterologist may create a cystogastrostomy with the use of endoscopic US, a procedure with
  • 12. 686  May-June 2016 radiographics.rsna.org a high success rate (29). However, if the collec- tion represents WON, adequate drainage may not be achieved with this approach owing to the nonliquefied components and, therefore, neces- sitating more aggressive débridement through the endoscope as a first-line therapy (Fig 11). Suggestions for Reporting When reviewing a patient’s history, it is important to note the time elapsed since the 1st day of ab- dominal pain, as this defines the time course used to stratify local complications. A statement about the presence or absence of necrosis should be made, and the location (peripancreatic, pancreatic, or both) and amount of necrotic gland (<30% or >30%) should be documented. Local complica- tions should be described in terms of location (lesser sac, anterior pararenal space, transverse mesocolon, etc), size, appearance, and presence or absence of a mature wall. Specifically, the contents of local complications should be described either as homogeneous with fluid attenuation (APFC or pseudocyst) or as having nonliquefied necrotic components (ANC orWON). Finally, the col- lection should be specifically named according to the revised Atlanta classification lexicon, with the subtype of pancreatitis and the number of weeks since the onset of abdominal pain (<4 or ≥4 weeks) taken into account (Fig 15).We sug- gest that the findings be succinctly summarized in the impression section of the report (eg, IEP or necrotizing pancreatitis with type and location of collection) and a statement that the revised Atlanta classification was used so that multidisciplinary team members recognize the expertise and the standardization of terminology. Conclusion Incorporation of the revised Atlanta classification system into everyday practice updates and stan- dardizes terminology, which facilitates accurate documentation of the range of imaging findings in acute pancreatitis. It is important to remember that pancreatitis-related collections are not always fluid filled, and evaluation for nonliquefied compo- nents is essential for differentiating collections that contain only fluid (APFCs and pseudocysts) from those that contain necrotic nonliquefied debris (ANCs andWON). In general, imaging findings combined with the time course of the disease allow clear differentiation between the collections and en- able stratification among different treatment plans, facilitating the radiologist’s seamless integration into a multidisciplinary team of gastroenterologists, intensivists, interventionalists, and surgeons. References 1. Bradley EL 3rd. A clinically based classification system for acute pancreatitis: summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11–13, 1992. Arch Surg 1993;128(5):586–590. 2. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1): 102–111. 3. The Pancreas Club, Inc. Revision of the Atlanta classifica- tion of acute pancreatitis. Available at: http://pancreasclub .com/wp-content/uploads/2011/11/AtlantaClassification.pdf. Published April 9, 2008. Accessed March 28, 2015. 4. Thoeni RF. The revised Atlanta classification of acute pan- creatitis: its importance for the radiologist and its effect on treatment. Radiology 2012;262(3):751–764. 5. BollenTL.Imagingofacutepancreatitis:updateoftherevised Atlanta classification. Radiol Clin North Am 2012;50(3): 429–445. 6. Sheu Y, Furlan A, Almusa O, Papachristou G, Bae KT. The revisedAtlantaclassificationforacutepancreatitis:aCTimag- ingguideforradiologists.EmergRadiol2012;19(3):237–243. Figure 15.  Decision tree for re- porting according to the revised Atlanta classification.
  • 13. RG  •  Volume 36  Number 3 Foster et al  687 7. Bollen TL, Besselink MG, van Santvoort HC, Gooszen HG, van Leeuwen MS. Toward an update of the Atlanta classifi- cation on acute pancreatitis: review of new and abandoned terms. Pancreas 2007;35(2):107–113. 8. DunnickNR,LanglotzCP.Theradiologyreportofthefuture: a summary of the 2007 Intersociety Conference. J Am Coll Radiol 2008;5(5):626–629. 9. Ellenbogen PH. BI-RADS: revised and replicated. J Am Coll Radiol 2014;11(1):2. 10. Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology 2013;144(6): 1252–1261. 11. Petrov MS, Windsor JA. Classification of the severity of acute pancreatitis: how many categories make sense? Am J Gastroenterol 2010;105(1):74–76. 12. Baker ME, Nelson RC, Rosen MP, et al. ACR Appropriate- ness Criteria acute pancreatitis. Ultrasound Q 2014;30(4): 267–273. 13. Singh VK, Bollen TL, Wu BU, et al. An assessment of the severityofinterstitialpancreatitis.ClinGastroenterolHepatol 2011;9(12):1098–1103. 14. Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung CL, Sibbald WJ. Multiple organ dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med 1995;23(10):1638–1652. 15. Spanier BW, Nio Y, van der Hulst RW, Tuynman HA, Dijkgraaf MG, Bruno MJ. Practice and yield of early CT scan in acute pancreatitis: a Dutch observational multicenter study. Pancreatology 2010;10(2-3):222–228. 16. Lenhart DK, Balthazar EJ. MDCT of acute mild (nonnecro- tizing)pancreatitis:abdominalcomplicationsandfateoffluid collections. AJR Am J Roentgenol 2008;190(3):643–649. 17. Sandrasegaran K, Tann M, Jennings SG, et al. Disconnec- tion of the pancreatic duct: an important but overlooked complication of severe acute pancreatitis. RadioGraphics 2007;27(5):1389–1400. 18. Kamal A, Singh VK, Akshintala VS, et al. CT and MRI assessmentofsymptomaticorganizedpancreaticfluidcollec- tionsandpancreaticductdisruption:aninterreadervariability study using the revised Atlanta classification 2012. Abdom Imaging 2015;40(6):1608–1616. 19. FreemanML,WernerJ,vanSantvoortHC,etal.Interventions for necrotizing pancreatitis: summary of a multidisciplinary consensus conference. Pancreas 2012;41(8):1176–1194. 20. Tüney D, Altun E, Barlas A, Yegen C. Pancreatico-colonic fistula after acute necrotizing pancreatitis: diagnosis with spiral CT using rectal water soluble contrast media. JOP 2008;9(1):26–29. 21. Kochhar R, Jain K, Gupta V, et al. Fistulization in the GI tract in acute pancreatitis. Gastrointest Endosc 2012;75(2): 436–440. 22. vanBaalMC,BollenTL,BakkerOJ,etal.Theroleofroutine fine-needle aspiration in the diagnosis of infected necrotizing pancreatitis. Surgery 2014;155(3):442–448. 23. Türkvatan A, Erden A, Türkoğlu MA, Seçil M, Yüce G. Imaging of acute pancreatitis and its complications. II. Complications of acute pancreatitis. Diagn Interv Imaging 2015;96(2):161–169. 24. Memiş A, Parildar M. Interventional radiological treatment in complications of pancreatitis. Eur J Radiol 2002;43(3): 219–228. 25. Shyu JY, Sainani NI, Sahni VA, et al. Necrotizing pancre- atitis: diagnosis, imaging, and intervention. RadioGraphics 2014;34(5):1218–1239. 26. vanSantvoortHC,BesselinkMG,BakkerOJ,etal.Astep-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010;362(16):1491–1502. 27. MadenciAL,MichailidouM,ChiouG,ThabetA,Fernández- delCastilloC,FagenholzPJ.Acontemporaryseriesofpatients undergoing open debridement for necrotizing pancreatitis. Am J Surg 2014;208(3):324–331. 28. WuBU,BanksPA.Clinicalmanagementofpatientswithacute pancreatitis. Gastroenterology 2013;144(6):1272–1281. 29. Varadarajulu S, Christein JD, Tamhane A, Drelichman ER, Wilcox CM. Prospective randomized trial compar- ing EUS and EGD for transmural drainage of pancreatic pseudocysts(withvideos).GastrointestEndosc2008;68(6): 1102–1111. This journal-based SA-CME activity has been approved for AMA PRA Category 1 Credit TM . See www.rsna.org/education/search/RG
  • 14. 1 Errata ERRATA May-June 2019 • Volume 39 • Number 3 Originally published in: RadioGraphics 2018; 38 (6):1609-1616 • https:// doi.org/10.1148/rg.2018180031 Rules and Regulations Relating to Roles of Non- physician Providers in Radiology Practices C. Matthew Hawkins Erratum in: RadioGraphics 2019:39(3):XXXX • https://doi. org/10.1148/rg.2019XXXXX Second paragraph, second column, p 1610: The sixth sentence should read as follows: “The authors of a review article emphasized that employing RAs increases physician supervision in nearly all clinical settings and that billing for services provided by RAs without ap- propriate supervision violates the False Claims Act.” Originally published in: RadioGraphics 2018; 32(2):1421–1440 • https://doi. org/10.1148/rg.2018180041 Radiation Dose Reduction at Pediatric CT: Use of Low Tube Voltage and Iterative Reconstruction Yasunori Nagayama, Seitaro Oda,Takeshi Nakaura, Akinori Tsuji, Joji Urata, Mitsuhiro Furusawa, Daisuke Utsunomiya,Yoshinori Funama, Masafumi Kidoh,YasuyukiYamashita Erratum in: RadioGraphics 2019:39(3):XXXX • https://doi. org/10.1148/rg.2019XXXXX First sentence, third full paragraph, p 1425: The sentence should read as follows: “Radiation output is proportional to the square of tube voltage but shows a linear relationship with tube current.” Originally published in: RadioGraphics 2016; 36(3):675–687 • https://doi. org/10.1148/rg.2016150097 Revised Atlanta Classification for Acute Pancreatitis: A Pictorial Essay Bryan R. Foster, Kyle K. Jensen, Gene Bakis, Akram M. Shaaban, Fergus V. Coakley Erratum in: RadioGraphics 2019:39(3):XXXX • https://doi. org/10.1148/rg.2019XXXXX Note,Table 1: The abbreviation for IEP should read as follows: “IEP = interstitial edematous pancreatitis.” Originally published in: RadioGraphics 2012; 32(2):437–451 • https://doi. org/10.1148/rg.322115032 Peritoneal and Retroperitoneal Anatomy and Its Relevance for CrossSectional Imaging Temel Tirkes, Kumaresan Sandrasegaran, Aashish A. Patel, Margaret A. Hollar, Juan G. Tejada, Mark Tann, Fatih M. Akisik, John C. Lappas Erratum in: RadioGraphics 2019:39(3):XXXX • https://doi. org/10.1148/rg.2019XXXXX First sentence, p 447: The first sentence should read as follows: “The retroperitoneum is divided into three distinct compartments: the posterior pararenal space, bounded by the transversalis fascia posteriorly; the anterior pararenal space, bounded by the parietal peri- toneum anteriorly; and the perirenal space, bounded by the perirenal fascia (Fig 12a, 12b).”