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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1649_Библиотеки_им_академика_М_И_Перельмана.pdf
Management of Acute Biliary Pancreatitis
141
Severe acute pancreatitis: clinical forms of different gravity. Neri V, Ambrosi
A, Fersini A, Tartaglia N, Lapolla F, Forlano I. Ann Ital Chir. 2013 Jan-
Feb; 84(1):47-53.
In: Acute Pancreatitis ISBN: 978-1-63485-229-6
Editor: Shane Copeland © 2016 Nova Science Publishers, Inc.
Chapter 7
RADIOLOGY OF ACUTE PANCREATITIS
AND ITS COMPLICATIONS
Kamil Zeleňák
1
*
, MD, PhD,
and Martin Števík
2
, MD, PhD
1
Jessenius Faculty of Medicine and University Hospital, Kollárova 2
Martin, Slovakia
2
University Hospital Kollárova 2, Martin, Slovakia
ABSTRACT
Acute pancreatitis (AP) is one of the most common diseases of the
gastrointestinal tract, leading to significant emotional, physical, and
financial burden for society. The diagnosis of acute pancreatitis is often
established by clinical symptoms and laboratory testing.
The latest revised Atlanta classification of acute pancreatitis was in
2012. This international consensus provides clear definitions to classify
acute pancreatitis using easily identified clinical and radiologic criteria.
This classification differentiates the two types of acute pancreatitis,
namely interstitial oedematous pancreatitis and necrotizing pancreatitis,
and defines the morphology seen on imaging of pancreatic and
peripancreatic collections that arise as complications of acute pancreatitis.
Severity is classified as mild, moderate or severe. Local complications are
peripancreatic fluid collection, pancreatic and peripancreatic sterile or
infected necrosis, pseudocyst and walled-off necrosis.
*
Corresponding Author address: Email: zelenak@jfmed.uniba.sk.
Kamil Zeleňák and Martin Števík
144
Imaging techniques commonly used for the diagnosis and severity
assessment of AP include abdominal ultrasound, contrast-enhanced
computed tomography (CECT), and magnetic resonance imaging (MRI).
CECT provides over 90% sensitivity and specificity for the diagnosis
of acute pancreatitis, which is why, together with MRI, it should be
reserved for patients in whom the diagnosis is unclear or who fail to
improve clinically. Computed tomography (CT) and MRI are comparable
in the early assessment of AP. Magnetic resonance imaging is useful for
patients with a contrast allergy and renal insufficiency.
Alongside treatment with drugs, supportive and surgical treatment,
interventional radiology has a unique place in indicated cases. Infected
pancreatic necrosis remains the most important indication for
intervention, to prevent the development of sepsis, and thus it is the most
common cause of death in acute pancreatitis.
Haemorrhagic complications are usually manifestations of the
progress of severe pancreatitis. Endovascular therapy remains the first-
line option for known arterial bleeding and visceral pseudoaneurysms.
Keywords: acute pancreatitis, scoring system, pancreatic necrosis,
peripancreatic collection, bleeding, visceral pseudoaneurysm
INTRODUCTION
Acute pancreatitis (AP) is a common medical condition with extensive
morbidity and mortality. Approximately 5% of patients with AP will die [23].
Gallstones and alcohol misuse are the main risk factors for acute
pancreatitis [33].
The incidence of acute pancreatitis varies between 4.9 and 73.4 cases per
100,000 worldwide. Acute pancreatitis is a sudden onset, primarily non-
infectious inflammatory disease of the pancreas. It is caused by inappropriate
intracellular activation of proteolytic enzymes and subsequent autodigestion of
the pancreatic parenchyma and surrounding tissues [20].
Even with increasing proportion of patients with severe AP, there has been
a significant decrease in organ failure adjusted mortality due to AP suggesting
improved management over years [1].
In accordance with the revised Atlanta classification, acute pancreatitis
can be diagnosed if at least two of the following three criteria are fulfilled:
abdominal pain (acute onset of persistent and severe epigastric pain, often
radiating to the back); serum lipase (or amylase) activity at least three times
the upper limit of normal; or characteristic findings of acute pancreatitis on
Radiology of Acute Pancreatitis and Its Complications
145
contrast-enhanced CT or, less often, MRI or transabdominal ultrasonography
[10].
CLASSIFICATION
The classification has prognostic and therapeutic implications. It has two
major roles. Staging the severity of the inflammatory process and detecting
complications, especially the identification and quantification of parenchymal
and peripancreatic necrosis. The diagnosis of acute pancreatitis is often
established by clinical symptoms and laboratory testing.
Stratification of patients with acute pancreatitis depends on the power of
the initial attack. Rapid assessment of the likelihood of severe course is
important to start an adequate treatment because any delay is burdened by
significant increases in morbidity and mortality [2, 48].
The clinical prognostic indicators mention the Ranson score, which takes
into account the biochemical parameters at the admission and during the first
48 hours of illness. Severe acute pancreatitis fulfils three or more of Ranson’s
criteria [39].
The first established radiological score was noted by Balthazar in 1985
[7]. The changes were described on a non-contrast enhanced computed
tomography scan looking for fluid collection and the degree of inflammatory
changes in the tissue, not for the evaluation of pancreatic necrosis.
Five years later, the Balthazar score was expanded by the computed
tomography severity index (CTSI) [8]. This combines the two computed
tomography prognostic indicators, i.e., the extent of necrosis and acute
inflammatory process. Another version of the CTSI designed by Mortelé
(modified CTSI) [36], adds parameters such as peripancreatic or vascular
changes and gastrointestinal involvement. A comparison of both
classifications is shown in (Table 1). Both the CTSI and modified CTSI
systems were able to predict the need for interventions with greater accuracy
than clinical systems [15].
The problem of radiological scoring systems based on the extent of
necrosis is the low resolution of the contrast computed tomography
examinations in the early days of the disease, which is crucial for the initiation
of therapy. The scores of De Waele et al. [20] includes the peripancreatic
inflammatory conditions and the extent of ascites, pleural effusion and others.
The advantage of this is that for these to be detected it is not necessary to
apply a contrast medium, they can be differentiated in the early days of the
disease. With a sensitivity of 100% and a specificity of 70.8% it is possible, 24
Kamil Zeleňák and Martin Števík
146
hours after admission, to predict severe acute pancreatitis with scores of 4 or
more [20, 43].
Table 1. Comparison of computed tomography severity
index (CTSI) – according to Balthazar [8] and Mortelé [36]
Balthazar CTSI
Mortelé CTSI
Pancreatic inflammation
Points
Grade
Points
Normal pancreas
0
A
0
Enlargement of the pancreas
1
B
2
Peripancreatic inflammation
2
C
One acute peripancreatitic fluid
collection
3
D
2
Two or more acute
peripancreatitic fluid collection
4
E
Extra pancreatic complications
2
Pancreatic necrosis
None
0
0
Less than 30%
2
2
30-50%
4
4
More than 50%
6
CTSI Score Grade
Mild pancreatitis
0-3
0-2
Moderate pancreatitis
4-6
4-6
Severe pancreatitis
7-10
8-10
The Atlanta classification of acute pancreatitis was most recently revised
in 2012 [10]. This international consensus provides clear definitions to classify
acute pancreatitis using easily identified clinical and radiologic criteria. On
admission it is important to identify patients with potentially severe acute
pancreatitis who require aggressive early treatment.
The most common latest the Atlanta classification (as revised in 2012) has
several aspects:
Depending on the severity of clinical manifestations and from the
morphological point of view acute pancreatitis is divided into three grades:
mild acute pancreatitis, moderately severe acute pancreatitis and severe acute
pancreatitis [9]. Mild acute pancreatitis (Figure 1) is without organ failure and
the absence of local or systemic complications. Patients with mild acute
Radiology of Acute Pancreatitis and Its Complications
147
pancreatitis usually do not require pancreatic imaging. The diagnosis is based
on clinical and laboratory findings.
Figure 1. Axial CT image of acute interstitial oedematous pancreatitis in a 47 year-old
man. The image shows homogeneous enhancement of an enlarged pancreatic
parenchyma (asterisk) without necrosis and mild peripancreatic fat stranding (arrows).
Grade C (Balthazar), modified CTSI 2 - mild acute pancreatitis.
Figure 2. Axial CT image of acute necrotizing pancreatitis (peripancreatic necrosis
alone) in a 79-year-old man. CT shows normal enhancing pancreas (asterisk)
Kamil Zeleňák and Martin Števík
148
surrounded by heterogeneous acute necrotic collections (arrows) with fluid and non-
liquid (fat) densities, suggestive of peripancreatic necrosis alone. This collection can
be observed in the left anterior pararenal space and the root of the transverse
mesocolon. Grade D (Balthazar), modified CTSI 4 - moderate acute pancreatitis.
Moderately severe acute pancreatitis is characterized by the presence of
transient organ failure or local or systemic complications in the absence of
persistent organ dysfunction lasting less than 48 hours (Figure 2).
Severe acute pancreatitis is characterized by persistent organ failure,
dysfunction lasting more than 48 hours (Figure 3).
Figure 3. Axial CT image. Acute necrotizing pancreatitis (pancreas gland and
peripancreatic necrosis) in a 47-year-old man. (A) The enlargement of the pancreatic head
and a poorly contrasted area (indicated by the white asterix) were observed. CT reveals
perfusion defect of approximately 50% at the head and body of the pancreas (white asterisk)
with preserved enhancement of tail white arrow), surrounded by heterogeneous acute
necrotic collections (black arrow). Significant fat necrosis can be observed in the lesser sac,
both anterior and posterior pararenal space and transverse mesocolon (arrows). A large
amount of ascites (AS) was observed. Walled-off necrosis in right posterior pararenal
compartment (black asterix). Grade E (Balthazar), 30% to 50% parenchymal necrosis;
modified CTSI 8, severe acute pancreatitis.
Radiology of Acute Pancreatitis and Its Complications
149
(B) Follow-up CT examination 26 days later. After operation without walled-off necrosis in
right posterior pararenal compartment, but progression of walled-off necrosis in
peripancreatic compartment was observed (>4 weeks) (white asterix) and pancreatic
necrosis (black asterix). CT depicts well-defined heterogeneous fully encapsulated
collection (white asterix). This was diagnosed as walled-off necrosis (WON).
In terms of time, acute pancreatitis is divided into early (less than one
week) and late stages (over one week). Morphologically there are two types of
acute pancreatitis, interstitial or oedematous pancreatitis (mild level) and acute
haemorrhagic necrotizing pancreatitis (severe stage) [21].
Necrosis of pancreatic parenchyma or peripancreatic tissues occurs in 10-
15% of patients. It is characterized by a protracted clinical course, a high
incidence of local complications, and a high mortality rate.
There are three subtypes of necrotizing pancreatitis: 1. Necrosis of both
pancreatic parenchyma and peripancreatic tissues (most common); 2. Necrosis
of only extrapancreatic tissue without necrosis of pancreatic parenchyma (less
common); 3. Necrosis of pancreatic parenchyma without surrounding necrosis
of peripancreatic tissue (very rare) [47].
Revised Definitions of Morphological Feature of Acute
Pancreatitis
Interstitial oedematous pancreatitis: Acute inflammation of the pancreatic
parenchyma and peripancreatic tissues, but without recognizable tissue
necrosis. CECT criteria: pancreatic parenchyma enhancement by intravenous
contrast agent. No findings of peripancreatic necrosis.
Necrotizing pancreatitis: Inflammation associated with pancreatic
parenchymal necrosis and/or peripancreatic necrosis. CECT criteria: lack of
pancreatic parenchymal enhancement by intravenous contrast agent and/or
presence of findings of peripancreatitic necrosis (ANC and WON).
Atlanta Classification of Fluid Collections
The 2012 revised Atlanta classification discerns four types of
peripancreatic fluid collections in acute pancreatitis depending on the content,
degree of encapsulation and time (Table 2).
Kamil Zeleňák and Martin Števík
150
Content: Fluid only in acute peripancreatic fluid collection (APFC) and
pseudocyst. Mixture of fluid and necrotic material in acute necrotic collection
(ANC) and walled-off-necrosis.
Degree of encapsulation: None or partial wall in APFC and ANC.
Complete encapsulation in pseudocyst and WON.
Time: Within 4 weeks: APFC and ANC. After 4 weeks: pseudocysts and
WON. It takes about 4 weeks for a capsule to form.
On CT, the discrimination between an APFC and ANC may be difficult,
especially in the first weeks and the term ‘indeterminate peripancreatic
collections’ can be used. All these collections may remain sterile or become
infected. Infection is rare during the first week.
Table 2. Revised Atlanta classification for imaging [21]
Pancreatitis
Collection
Infection
Less than 4 weeks
Interstitial oedematous
pancreatitis
APFC
+/- infection
Necrotizing pancreatitis
PNPFC
Parenchymal necrosis
+/- infection
Peripancreatitis necrosis
Mixed necrosis
More than 4 weeks
Interstitial oedematous
pancreatitis
Pseudocyst
+/- infection
Necrotizing pancreatitis
WOPN
+/- infection
APFC – acute peripancreatitic fluid collection.
PNPFC – post-necrotic pancreatic fluid collection.
WOPN – walled-off pancreatic necrosis.
1. APFC (Acute Peripancreatic Fluid Collection)
Peripancreatic fluid associated with interstitial oedematous pancreatitis
with no associated peripancreatic necrosis. This term applies only to areas with
peripancreatic fluid seen within the first 4 weeks after onset of interstitial
oedematous pancreatitis without the features of a pseudocyst. CECT criteria:
occurs in the setting of interstitial oedematous pancreatitis. Homogeneous
collection with fluid density. Confined by normal peripancreatic fascial planes.
No definable wall encapsulating the collection. Adjacent to pancreas (no
intrapancreatic extension).