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Radiologic Diagnosis andStaging ofSevere Acute Pancreatitis

Yoshihisa Tsuji

Department of General Medicine, Center for Graduate Medical Education, Sapporo Medical University, Sapporo, Hokkaido¯ , Japan

Introduction

The role of imaging is important in diagnosis and evaluation of severity in patients with known or suspected acute pancreatitis. Common imaging techniques for the evaluation of the pancreas include transabdominal ultrasonography (US), computed tomography (CT), and magnetic resonance imaging (MRI). Angiography and positron emission tomography (PET)- CT are sometimes used to diagnose special complications in acute pancreatitis patients. This chapter deals with these imaging techniques in the diagnosis of local and systemic inf lammation associated with acute pancreatitis.

Classification ofAcute Pancreatitis

Acute pancreatitis represents a spectrum of inflammatory disease ranging from clinically mild to severe acute pancreatitis[1]. In recent years a radiological approach has been commonly used to diagnose acute pancreatitis and evaluate severity. For these purposes, CT is one of the most popular methods. Abdominal CT has been commercially available since the 1970s.

In 1983, Kivisaari etal. reported that pancreatic necrosis in acute pancreatitis could be diagnosed using CT[2]. Bradley etal.[3] and Johnson etal.[4] also reported the usefulness of CT in diagnosis of pancreatic necrosis in acute pancreatitis patients, in 1989 and 1991, respectively. These studies regarded pancreatic necrosis as one of the most important factors in predicting a poor prognosis (Table23.1).

In contrast, based on broadening of inflammation, Balthazar et al. [5] established a CT grading system to define the severity of acute pancreatitis in 1985. This is called Balthazar’s CT grade, and it became one of the

most popular image-

based grading systems of severity of acute pancreatitis. It was partially modified in 2002[6]. In 1985 the Balthazar system classified acute pancreatitis into five grades: A— normal, B— focal or diffuse enlargement of the pancreas, C— peripancreatic inflammation with intrinsic pancreatic abnormalities, D— intra- or extrapancreatic fluid collections, and E— two or more large collections of gas in the pancreas or retroperitoneum. In the 2002 version, grades D and E were modified: D— single fluid collection and E— two or more fluid collections and/or retroperitoneal air, respectively.

The two concepts that assist in diagnosis— local pancreatic damage and evaluation of broadening of inflammation— were combined into the CT severity index to predict prognosis (see section on CT severity index later in this chapter).

According to these moves to diagnose and evaluate acute pancreatitis using CT, a newer classification of acute pancreatitis was discussed at the Atlanta conference in 1992[7]. In Atlanta, following previous symposia[8–10], severity of acute pancreatitis was classified into two grades: mild and severe. In this classification, severe acute pancreatitis was associated with organ failure and/or local complications, such as pancreatic necrosis, pancreatic fluid collection, acute pseudocyst, or pancreatic abscess. Since it was considered that CT could diagnose these local complications accurately, descriptions of the Atlanta classification were largely devoted to diagnostic criteria of local complications on CT. Following this symposium, radiological findings associated with acute pancreatitis were described in medical reports based on these terminological definitions.

The Atlanta classification was universally applied for two decades from 1992. During these two decades, two important insights were reported. First, Casas et al. reported that the early CT, which was performed within

The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Fourth Edition. Edited by Hans G. Beger, Markus W. Büchler, RalphH. Hruban, Julia Mayerle, John P. Neoptolemos, Tooru Shimosegawa, Andrew L. Warshaw, David C. Whitcomb, and Yupei Zhao. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/beger/thepancreas4e

Table23.1 Diagnostic criteria ofpancreatic necrosis andtheir accuracy.

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Scanning

Study n Timing of performing CT

protocol Diagnostic criteria

Classification ofAcute Pancreatitis 209

Accuracy for diagnosis of

pancreatic necrosis

Sensitivity Specificity

Kivisaari 1983[2] 28 <1day from

Block 1986[29] 77 – CE-

Nuutinen 1988[30] 28 – NC + CE-

Bradley 1989[3] 37 <2days from

Larvin 1990[31] 60 <7days from

Johnson 1991[4] 13 <3days from

Bradley 1993[7]

Casas 2004[11] 184 <3days from the onset CE- CT – 53 90

Takeda 2005[27] 102 <7days from the onset CE-

Tsuji 2007[32] 30 <3days from the onset Perfusion CT Comparison of hepatic

Spanier 2010[33] 166 – – – 0 –

Tsuji 2014[34] 48 <3days from the onset CE-

Yadav 2015[35] 32 <3days from the onset Perfusion CT PBF <23 mL/100 mL/min 87.5 100

Pienkowska 2016[36]

administration

– – CE- CT <50 HUb or comparison

79 <1day from the onset Perfusion CT Permeability

NC + CE- CT <15 HU

CT – 85 50

CT <30 HU

CE-

CT <40 HU

CT <30 HU

CE-

CT Lack of enhancement 100 100

CE-

CT Lack of enhancement – –

CT Lack of enhancement 74.5 (64–82)

NC + CE- CT 77.5 (64–91)d88 (81–97)

CE + sub- CT <15 HU

to splenic enhancement

perfusion

mL/100 mL/min

<40

100 –

– –

100 95.3

87.5 (78–97)

91 (82–100)d94.7 (89–100)

100 84.2

NC: noncontrast; CE: contrast- enhanced; sub- CT: subtraction color map based on duel energy CT; PBF: pancreatic blood flow; –: not described.

Difference of CT values between pre- and postinjection of contrast agent.

CT values of postinjection of contrast agent.

Atlanta criteria.

Average values among three reviewer (minimum–maximum).

3 days from the onset, could not diagnose pancreatic necrosis accurately [11]. Second, a new concept, “walled- off necrosis (WON),” was proposed [12,13]. Early pancreatic complications (e.g., pancreatic and peripancreatic necrosis) could develop WON 4weeks later than the onset. The concept of “WON” has made meanings of pseudocysts different (Table23.2). Our improved understanding of the pathophysiology of organ failure and necrotizing pancreatitis and their outcomes, as well as improved diagnostic imaging, have made it necessary to revise the Atlanta classification.

The Atlanta classification was also revised in 2012[14]. According to this classification of acute pancreatitis, known as the “revised Atlanta classification,” the severity of acute pancreatitis is categorized into three groups: mild, moderate severe, and severe. In patients without

local and systemic complication, the severity is judged to be mild. Patients with local complication without organ failure or transient organ failure which can be controlled within 48 hours from induction of treatment are classified in the moderate severe group. Patients with organ failure that resists treatment resulting in persistence for 48 hours or more are classified as severe (Table23.2).

At the same time as the revised Atlanta classification, the determinant- based classification [15] was also published by another group. As with the revised Atlanta classification, the aim of this classification was to revise the original Atlanta classification. However, the determinantbased classification regards (peri)pancreatic necrosis as the more important factor to predict prognosis, compared to the revised Atlanta classification. According to determinant- based classification, the severity of acute

Table23.2 Diagnosis oflocal complications oncriteria.

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Terminology on Image on CT

Pancreatic Heterogeneous and

nonfluid density

Time from onset Pathology Late complicationAtlanta criteria

None None or less <3days Ischemic tissue Healing without

None <4weeks Pancreatic necrosis WON

Pancreatic necrosis

Revised Atlanta criteria

Determinantbased criteria Location Density Wall perfusion

ANC (Peri)

Pancreatic necrosis

Peripancreatic Fat necrosis

Pancreatic fluid collection

Acute pseudocyst PPC Well defined ≥4weeks

APFC Not described Homogeneous fluid

density

Inflammatory tissue Resolving

Sterile fluid PPC

Pancreatic abscess Infected fluid

WON Heterogeneous with

fluid and nonfluid density

ANC, acute necrotic collection; APFC, acute pancreatic fluid collection; PPC, pseudocyst; WON, walled- off necrosis.

Sterile WON

Infected

necrosis or WON

Radiographic Diagnosis ofSevere Acute Pancreatitis 211

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pancreatitis is categorized into four groups: mild, moderate, severe, and critical. If the patient has neither (peri) pancreatic necrosis nor organ failure, severity is judged to be mild. The patient with sterile (peri)pancreatic necrosis and/or transient organ failure is classified as moderate. The patient with infected necrosis or persistent organ failure (more than 48 hours from start of treatment) is classified into the severe group. The patient with both infected necrosis and persistent organ failure is classified into the critical group (Table23.2).

Between the revised Atlanta and determinant- based classifications, there is a difference with regard to the radiological definition of pancreatic necrosis. According to determinant- based classifications, (peri)pancreatic necrosis is nonviable tissue without a radiologically defined wall. In contrast, the revised Atlanta classification makes categorizes pancreatic necrosis into two types according to a diagnosis of well- defined wall: acute necrotic collection (ANC) and WON (Table23.2). In the determinantbased classification, there is no description with regard to necrotic tissue with radiologically well- defined wall, which was categorized into “acute pseudocyst or pancreatic abscess” and “pancreatic pseudocyst or walled- off necrosis” in the Atlanta and revised Atlanta classifications, respectively. Thus, it appears that the concept of pancreatic necrosis in the determinant- based classification is not the same as that in the revised Atlanta classification.

In both the revised Atlanta and determinant- based classifications, the development of persistent organ failure (48 hours or more from start of treatment) is needed to diagnose severe or critical acute pancreatitis. Thus, in the emergency room we can use only two grades of severity: mild or moderate. From this point of view, a

patient with moderate acute pancreatitis is potentially at high risk of developing severe or critical acute pancreatitis. Accurate diagnosis of pancreatic necrosis is one of the most important factors to perform in the emergency room for appropriate triage based on the severity of recent classifications.

Radiographic Diagnosis ofSevere Acute Pancreatitis

Two major types of acute pancreatitis are known: acute edematous and necrotizing pancreatitis [14]. Since the prognoses and strategies of treatment of these two are totally different, it is necessary to diagnose them accurately.

Acute Edematous Pancreatitis

According to Klöppel[16], the pancreas is enlarged without necrosis on gross pathology in acute edematous pancreatitis, although microscopic areas of parenchymal fat necrosis may also be found. Lack[17] stated that hemorrhage and intraparenchymal necrosis is absent in the pancreas. Importantly, in acute edematous pancreatitis, where fat necrosis does not come into contact with a blood vessel, it does not damage the vessel wall, leading to macroscopic pancreatic necrosis [16]. Thus contrast enhancement of pancreatic parenchyma is usually normal on contrastenhanced CT (CE- CT). In addition, the revised Atlanta classification[14] described that CE- CT shows pancreatic swelling with relatively homogeneous enhancement in acute edematous pancreatitis (Fig.23.1).

Figure23.1 Acute edematous pancreatitis. (a) Contrast- enhanced CT shows enlargement of pancreas (P). At the same time as (a),

perfusion CT was obtained. (b) Tissue blood flow was demonstrated based on the left- sided scale bar. Pancreatic blood flow was red- yellow (about 40 mL/100 g/min), which indicates that pancreatic blood flow was high.

Radiologic Diagnosis andStaging ofSevere Acute Pancreatitis

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212

In the Atlanta classification[7], the macroscopic feature of mild acute pancreatitis was interstitial edema. Therefore, in those days, mild acute pancreatitis was nearly equal to acute edematous pancreatitis. One of the important things to note is that the revised Atlanta classification[14] changes the definition of mild acute pancreatitis to “pancreatitis with no organ failure and no local or systemic complications.” In the revised Atlanta classification, local complications are redefined as acute peripancreatic fluid collection (APFC), pancreatic pseudocyst (PPC), acute necrotic collection (ANC), and walled- off necrosis (WOF). Thus, using the revised Atlanta, acute edematous pancreatitis with APFC, one of the local complications, is classified into moderate severe acute pancreatitis, not mild. The prognosis of patients with acute edematous pancreatitis is much better than that of those with local complication.

Acute Necrotizing Pancreatitis

Approximately 2–10% of acute pancreatitis patients develop necrosis of pancreatic parenchyma and/or peripancreatic tissue [14,18]. Both in the Atlanta and the revised, acute necrotizing pancreatitis is defined as “acute pancreatitis with pancreatic necrosis which involves pancreatic parenchymal necrosis and/or peripancreatic fat necrosis.” Reports put the mortality rate for acute pancreatitis patients with pancreatic necrosis at roughly 30%[19].

Development of pancreatic parenchymal necrosis consists of three steps: acinar injury, vascular injury, and tissue injury. The initial pathway in the development of pancreatitis is ectopic activation of trypsinogen in acinar cells and/or activation of macrophages [20–23] or neutrophils[24]. The activation of trypsinogen in acinar cells leads to the acinar cells being destroyed, followed by releases of trypsin and damageassociated molecular pattern molecules (DAMP) [25] into the pancreatic vessels. Vascular epithelial cells are injured by the released trypsin and/or DAMP, resulting in damage to the coagulant–fibrinolytic system of the endothelial cells. In combination with this endothelial damage, periarterial fat necrosis, interstitial edema, and/or bleeding due to inflammation reduces tissue perfusion by compressing vessels. If this reduction of perfusion continues and/or ischemic–reperfusion damage occurs, serious tissue damage often develops, leading to acute necrotic collection (ANC)[26,27]. At 4weeks or more later, ANC may develop WON. Since ANC and WON are irreversible, attempts to prevent the development of ANC or WON should be started based on a diagnosis of pancreatic ischemia[28] (see sections on acute necrotic collection and walled- off necrosis later).

To diagnose pancreatic necrosis (pancreatic ischemia,

ANC, and WON), CE-

CT, MRI, or CE- US are used. According to CE- CT criteria in the revised Atlanta classification, acute necrotizing pancreatitis is diagnosed based on lack of pancreatic parenchymal enhancement by intravenous contrast agent and/or presence of peripancreatic necrosis (Table23.1)[2–4,7,11,27,29–36].

Diagnosis ofLocal Complications ofAcute Pancreatitis

As was described earlier, local complications are divided into four types: APFC, ANC, WON, and PPC in the revised Atlanta classification.

Acute Peripancreatic Fluid Collection

In the Atlanta classification[7], pancreatic fluid collections occurred early in the course of acute pancreatitis, were located in or near the pancreas and always lacked a wall of granulation or fibrous tissue. The precise composition of such collections was not known pathologically. Instead of the term “pancreatic fluid collections”[7], the use of the term APFC was suggested in the revised Atlanta classification[14]. APFC is peripancreatic fluid association with interstitial edematous pancreatitis and without necrosis. In CE- CT, APFC is a homogeneous collection with fluid density, without abnormal peripancreatic fascial planes, without defined wall encapsulating the collection, and without intrapancreatic extension (Table23.2, Fig.23.1).

Acute Necrotic Collection

ANC includes parenchymal necrosis of pancreas and peripancreatic fat necrosis. Thus, acute pancreatitis with ANC is the same as acute necrotizing pancreatitis. A collection contains variable amounts of both fluid and necrotic tissues. As was previously described, ANC is a pre- stage of developing WON. The border between ANC and normal tissue is gray (Fig.23.2).

Parenchymal necrosis of pancreas appears as a low attenuation or non- enhancing area on CE- CT [4,5,37]. Early studies reported that CE- CT was highly accurate for the detection of pancreatic necrosis [3,4,29]. These studies mostly included surgical cases, so very few patients in the early stage of acute pancreatitis were included. Four previous studies reported the accuracy of CE- CT in predicting pancreatic necrosis in the early stages of acute pancreatitis [11,33,34,38]. One study showed that pancreatic necrosis was not detected in any of 49 patients with acute pancreatitis on CE- CT

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Diagnosis ofLocal Complications ofAcute Pancreatitis 213

Figure23.2 Acute necrotizing pancreatitis and its natural history. Due to serious complications of acute pancreatitis, this patient had

three CT scans during the course of the disease. Contrast- enhanced CT shows homogeneous enhancement of pancreas at day 1 (a). On day 8 (b), enhancement of pancreas was markedly reduced, so this case was diagnosed as acute necrotizing pancreatitis. (c) On day 36, the scan shows acute necrotic collection (ANC) and altered walled-

performed within 72 hours of onset (sensitivity: 0%)[33], while the three other studies [11,34,38] showed that CE- CT had a sensitivity of 63%, 72%, and 75%, respectively, for the early phase of acute pancreatitis (within 1day of admission or 72 hours of onset).

As Klöppel described previously [16], pancreatic inflammation can reduce pancreatic blood flow, resulting in development of pancreatic necrosis. Using angiography, Takeda also showed that pancreatic parenchyma with vasospasm of the intrapancreatic artery develops parenchymal necrosis with high ratio [27]. Perfusion CT[39,40], which can measure parenchymal blood flow accurately, has shown promise as a method that can accurately detect pancreatic necrosis at an early stage of acute pancreatitis with an estimated sensitivity of

off necrosis (WON), which was surrounded by a well- defined wall.

88–100% and specificity of 84–100%[32,35,36] (Fig.23.3). Perfusion CT can differentiate reversible from irreversible ischemic tissue, and thus has been used widely for diagnosing acute brain stroke (Fig. 23.1). According to Yadav etal.[35], pancreatic parenchyma with poor blood flow (cutoff value about 20 mL/100g/min or less and normal pancreas 100 mL/100g/min or more) could develop pancreatic necrosis with high ratio. At 24 hours from onset, Pienkowska et al. [36] showed that perfusion CT can predict development of pancreatic necrosis accurately. This suggests that the parenchymal blood flow is decreased even at an early stage of acute pancreatitis in areas of impending necrosis (Fig.23.4 and23.5).

Dynamic contrast- enhanced magnetic resonance

imaging (CE- MRI)[41] may be an alternative to CE- CT

Radiologic Diagnosis andStaging ofSevere Acute Pancreatitis

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214

with liquid and nonliquid density with varying degrees of loculations [14]. Ultrasound (both percutaneous and endoscopic) or MRI is better for diagnosing the heterogeneity of WON compared to CE-

CT, because the identification of the liquid area in necrosis by MRI or ultrasound is more accurate than that by CE- CT.

Compared to ANC, WON has well- defined walls at marginal zone of necrosis, and therefore the border is clear. WON develops liquefaction of necrotic area heterogeneously and gradually[17]. Some areas of WON have inner walls, and WON can thus be separated into various sizes. In addition, WON develop in many areas, side by side or separately. Therefore, in acute pancreatitis patients with local complications, there is a possibility that many areas of WON will develop in the abdominal cavity.

In cases of suspected ANC/WON infection, rapid enlargement of the necrotic area, inflammatory changes in the neighboring fat, gas in the necrotic area, and surrounding paralytic ileus may help to diagnose the location of the infection (Fig.23.6). One study suggests that

CT may be useful in identifying infected WON[42],

PETalthough it is expensive.

Figure23.3 Difficulty in identifying pancreatic parenchymal

necrosis using conventional CT. (a) Using contrast(day 1), regional necrosis on the pancreatic head was not identified (arrowheads). (b) However, perfusion CT showed markedly reduction of pancreatic perfusion. (c) The poor perfusion area on perfusion CT (b) was concordant with an area of pancreatic necrosis at autopsy.

enhanced CT

for detecting pancreatic necrosis. Indeed, MRI has certain advantages over conventional CE- CT, including greater sensitivity in detecting ischemia. Moreover, when MR angiography is performed in conjunction with MRI, assessment of vessel patency is also possible.

Walled-

off Necrosis

WON is defined as a mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has a well- defined wall [12–14]. It arises secondary to ANC and usually occurs at >4weeks after onset of acute pancreatitis. On CE- CT, WON often appears heterogeneous,

Pancreatic Pseudocyst

It should be noted that the definition of the term PPC has recently changed. Previously, PPC included both WON and encapsulating fluid [7]. In the latest international classification, the revised Atlanta[14], PPC is redefined as an encapsulating collection of fluid with a well- defined inflammatory wall. PPC usually occurs more than 4weeks after onset, as well as WON. Any solid region is not identified as PPC, thus (endoscopic) US or MRI is useful to diagnose it (Fig.23.7).

Radiologic Staging ofSevere Acute Pancreatitis

The concept of radiologic staging of severity of acute pancreatitis is based on two important findings: extent of inflammation and necrosis (ANC/WON).

CT Severity Index

Combining the findings of broadening of inflammation and local pancreatic damage on CT, the CT severity index (CTSI) was published in 2002. In the CTSI, Balthazar CT grade A (normal pancreas) scores 0, grade B (enlargement of pancreas) scores 1, grade C (inflammatory changes in pancreas and peripancreatic fat) scores 2, grade D (single fluid collection) scores 3, and grade E (two or more poorly defined fluid collections)

Limitations andPitfalls ofRadiologic Diagnosis ofAcute Pancreatitis 215

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(d)

Figure23.4 Reversible ischemia and necrosis in early stage of severe acute pancreatitis. (a) Contrast- enhanced CT (day 1) showed a lack

of enhancement of the pancreatic tail (area surrounded by dotted line). (b) Perfusion CT showed a poorly perfused area in the pancreatic tail, which was smaller than the area with lack of enhancement on contrast- enhanced CT. (c) The area with poor perfusion in the perfusion CT developed pancreatic necrosis. (d) Based on these findings, the schema shows that the marginal zone of pancreatic necrosis could have been reversible ischemia.

scores 4. The pancreatic condition is independently evaluated: no pancreatic necrosis on CT scores 0, pancreatic necrosis less than/equal to 30% of pancreas scores 2, >30–50% scores 4, and >50% scores 6. Grading severity is based on a CTSI score of 0–10: mild (score 0–3), moderate (score 4–6), and severe (score 7–10)[5,6]. The CTSI was modified in 2004 by Mortele etal. (MDThe MD- CTSI resulted in higher interobserver agreement ratio, correlation with length of hospital stay, need for invasive therapy, incident organ failure, and the occurrence of infection (Table23.3).

Japanese CT Severity Index

In the latest Japanese definition of severe acute pancreatitis[44], Hiroto et al. established the JPN- CT severity score. In the definition, severe acute pancreatitis can be diagnosed either by the laboratory/clinical severity criteria or JPN- CT. The case mortality rate of patients with severe acute pancreatitis diagnosed by JPN- CT score

CTSI)[43].

was 14.8%. The case fatality of severe acute pancreatitis that fulfilled JPN-

CT severity criteria (severity score ≥2

points) was as high as 30.8%.

Limitations andPitfalls ofRadiologic Diagnosis ofAcute Pancreatitis

Diagnosis ofEarly Necrosis ofPancreatic Parenchyma

The accuracy of CE- CT to diagnose pancreatic parenchymal necrosis within 3 days of onset is not adequate [11,37]. One potential explanation for this disappointing performance of CE- CT is that the attenuation of pancreatic parenchymal necrosis is similar to that of viable enhancing parenchyma on CE- CT in the early stages of acute pancreatitis, and the CT attenuation of pancreatic necrosis decreases over time as nonviable parenchyma liquefies[12,31]. Moreover, because the CT

Radiologic Diagnosis andStaging ofSevere Acute Pancreatitis

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216

(d)

Figure23.5 Tissue hemorrhage makes it difficult to diagnose necrosis using contrast- enhanced CT alone. (a) Noncontrast CT showed

elevation of CT values in pancreatic body. (b) On CE- CT alone, it is difficult to judge whether the elevation of CT value of pancreatic parenchyma was due to hemorrhage or enhancement by contrast agent. (c) Perfusion CT showed that pancreatic blood flow of the whole pancreatic body was extremely low. These findings show that the pancreatic body had already developed necrosis on day 2. (d) The poorly perfused area with slight elevation of CT values on noncontrast CT was concordant with the area with later necrosis.

attenuation of pancreas may be altered by hemorrhage in necrosis or fatty infiltration, evaluation of regional variability in pancreatic enhancement becomes difficult with CE- CT. Another reason why CE- CT may not be accurate in predicting parenchymal necrosis in the early stages may involve the difficulty of evaluating the effectiveness of contrast- enhanced material. Since the border of early parenchymal necrosis that is included in the ANC is not clear, selecting specific of areas with suspicious parenchymal necrosis in the case of early acute pancreatitis

poses difficulties, in contrast to analyses of enhancements in well- defined lesions, such as a WON.

Although the detection of pancreatic parenchymal necrosis with CT imaging has led to the improved prognostic stratification of patients using the CT severity index [45], the inaccurate prediction of parenchymal necrosis using CE- CT and its large interobserver variability[43,46] may also lead to recent recommendations questioning the routine use of CT at an early stage of acute pancreatitis[47,48].

Limitations andPitfalls ofRadiologic Diagnosis ofAcute Pancreatitis 217

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(d)

Figure23.6 Infected walled- off necrosis (WON). (a) Presented case has WON on contrast- enhanced CT. (b) Most of the WON on the

pancreas body and tail was replaced with gas, due to infection. In the gas cavity of WON, the inner wall (arrowhead) was detected. (c)Percutaneous ultrasound showed high spotty areas due to gas in WON. (d) Surgical treatment was performed and a part of the inner wall (arrowhead) was shown in the cavity. The patient recovered 6months later.

Despite the advantages discussed earlier, MRI is underused in the evaluation of patients with severe acute pancreatitis. This underutilization can be attributed to practical considerations— patients with severe acute pancreatitis have difficulty withstanding the lengthy MRI procedure. In addition, removal of all the magnetic instruments (e.g., sphygmomanometer, saturation monitor, multiple infusion pumps, etc.), which cannot be taken away from patients with severe acute pancreatitis even for a short period, must be done before the procedure is performed.

Nephrotoxity of Contrast Material of CE- CT and CE- MRI

One of important systemic complications of acute pancreatitis is acute renal failure. Because CE- CT and dynamic CE- MRI has some nephrotoxicity, use of dynamic CE- MRI and CE- CT should be decided with care [41]. Perfusion CT is obtained from analysis of blood flow after a bolus injection of much less contrast materials (approximately 30–40%) than those used for conventional CE- CT[49]. Therefore, the nephrotoxity of

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