Acute pancreatitis is most commonly caused by gallstones

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1 CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2008;6: CLINICAL IMAGING Imaging of Acute Pancreatitis and Its Complications DESIREE E. MORGAN Department of Radiology, University of Alabama at Birmingham, Birmingham, Alabama Patients with acute pancreatitis may present with mild or severe disease, the latter comprising a minority of cases but accounting for most of the morbidity and mortality associated with this disease. Contrast-enhanced computed tomography is the mainstay of imaging patients with acute pancreatitis and is widely used in both the community and academic settings. A variety of retroperitoneal morphologic changes are readily depicted, and the correct assessment of these abnormalities is imperative for management. The purpose of this review is to describe the imaging evaluation of patients with acute pancreatitis by using the 1992 Atlanta Symposium classification and definitions to describe local complications depicted on contrast-enhanced computed tomography. Correlation with the proposed revision of Atlanta Symposium definitions set forth by the Acute Pancreatitis Working Group will be discussed. Acute pancreatitis is most commonly caused by gallstones or ethanol, with less common etiologies including tumor, trauma, hyperlipidemia, medications, and iatrogenic injuries incurred during endoscopic retrograde cholangiopancreatography and surgery. Symptoms are often nonspecific and include nausea, vomiting, and epigastric pain. On physical exam, patients present with abdominal distention, and when the acute pancreatitis is clinically severe, hypotension or tachycardia may be present. More specific clinical signs including Cullen s (periumbilical ecchymosis) or Grey Turner sign (flank ecchymosis) may indicate hemorrhagic acute pancreatitis; however, these findings may be present in other clinical scenarios such as Grey Turner sign noted in patients with a ruptured abdominal aorta or intra-abdominal hemorrhage caused by trauma. Typical laboratory abnormalities indicating acute pancreatitis are serum amylase and lipase elevation and, if biliary in origin, ALT elevation. Other indicators of acute inflammation have been measured in patients with acute pancreatitis and include C-reactive protein, procalcitonin, interleukin-6, and tumor necrosis factor; these are generally used in specialized centers or during research and are not commonly used to make the diagnosis of acute pancreatitis in the U.S. The Atlanta Symposium convened in and was composed of a panel of pancreatic experts charged with deriving a common language to describe acute pancreatitis and the associated morphologic complications. The common language was proposed to allow better comparison of study populations. The complications defined by the panel of experts are readily depicted with imaging, especially intravenous contrast-enhanced computed tomography (CECT). Also during that conference, recommended imaging protocols were proposed. However, during the last decade, an increase in clinically successful supportive measures in patients with acute pancreatitis in addition to emerging techniques for retroperitoneal drainage occurred, 4,5 and a deficiency in the Atlanta Symposium classification 6 8 specifically pertaining to the complex fluid collections arising from pancreatic necrosis that evolved over time was noted. Hence in May 2007, the Acute Pancreatitis Classification Working Group met to revise the definitions set forth in the Atlanta Symposium (M. Sarr, personal communication, January 2008). The clinical definition of acute pancreatitis requires 2 of 3 of the following features: abdominal pain suggestive of pancreatic origin, level of serum amylase or lipase greater than or equal to 3 times normal, and characteristic findings on CECT. This inclusion of CECT findings in the definition of acute pancreatitis is likely due to widespread increased utilization in both community hospitals and tertiary referral centers in the evaluation of patients with acute abdominal pain. According to the proposed revision, disease severity of acute pancreatitis should be based on clinical parameters during the first week and thereafter should be based on morphologic parameters depicted with imaging. Clinical Severity Nonsevere acute pancreatitis is the new term suggested to replace mild acute pancreatitis (Figure 1). Histologically, the retroperitoneal inflammation in these patients is limited to interstitial edema of the pancreas and micronecrosis. Clinically, the patients improve in hours and have no multisystem organ failure. In the past, prognosticators of disease severity including Ranson score less than 3, Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II score less than 8, and computed tomography severity index (CTSI) less than 3 predicted an uncomplicated course in patients with acute pancreatitis. In the past, no imaging of patients with suspected mild pancreatitis was deemed necessary other than ultrasound to evaluate for gallstones as a potential etiology. On CECT, mild pancreatic swelling and minimal peripancreatic wispy inflammatory changes are characteristic of the mild or nonsevere form of acute pancreatitis morphologically. Abbreviations used in this paper: APACHE, Acute Physiology, Age, and Chronic Health Evaluation; CECT, contrast-enhanced computed tomography; CTSI, computed tomography severity index; MRI, magnetic resonance imaging; WOPN, walled off pancreatic necrosis by the AGA Institute /08/$34.00 doi: /j.cgh

2 1078 MORGAN CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 6, No. 10 Figure 1. Mild (nonsevere) acute pancreatitis. A 36-year-old woman presented with acute onset of abdominal pain. Axial CECT image shows a small amount of inflammatory stranding (arrow) extending from the tail of pancreas, consistent with acute peripancreatic fluid collection. Visualized portions of the glandular tissue are enhancing normally. Figure 3. Subacute severe pancreatitis. A 52-year-old man presented on transfer from an outside hospital approximately 10 days after onset of acute pancreatitis. (A) Axial CECT through the body region of the pancreas demonstrates partial enhancement of the pancreatic neck (arrow), with heterogeneous low density replacing the remainder of the pancreas at this level. (B) Slightly more inferiorly at the uncinate level, there is partial granulation of the wall, with internal septations seen in the complex collection. The inflammatory exudate has also broken through Gerota s fascia and is in the perirenal space bilaterally. This patient has greater than 50% glandular necrosis and fluid collections in 2 regions, resulting in a CTSI of 10. Figure 2. Severe acute pancreatitis. (A) Axial CECT image through the pancreatic body and tail region shows edema of the tail (arrow), with low attenuation replacing the pancreatic parenchyma (short arrows) anterior to the splenic vein. (B) Slightly more inferiorly, normal enhancement is seen in the pancreatic head region (arrow). There is a large amount of peripancreatic retroperitoneal fluid as well as a small amount of ascites and anasarca. Severe acute pancreatitis retains the same name. Histologically, in patients with severe acute pancreatitis, there is confluent acinar cell and vascular macronecrosis, with or without main or side branch pancreatic duct disruption and adjacent retroperitoneal fat necrosis. Clinically, patients with severe acute pancreatitis have local complications in the retroperitoneum produced by the pancreatic exudates and may develop multisystem organ failure, most commonly renal, pulmonary, or cardiovascular in origin. Clinical prognosticators of Ranson score greater than 3, APACHE II greater than 8, and CTSI greater than 3 define this population. On CECT, patients with severe acute pancreatitis (Figure 2) typically exhibit larger amounts of peripancreatic retroperitoneal fluid that might extend throughout the anterior pararenal space into the transverse mesocolon or mesenteric root and affect adjacent bowel structures (stomach, ascending, and descending colon). In addition, these patients are at increased risk for developing pancreatic necrosis, readily depicted on CECT as geographic areas of low attenuation replacing the pancreatic parenchyma.

3 October 2008 IMAGING OF ACUTE PANCREATITIS AND ITS COMPLICATIONS 1079 Figure 5. Acute interstitial edematous pancreatitis. Axial CECT image through the mid pancreas reveals obscuration of the normal fatty interdigitation of the pancreatic parenchyma in the neck and body region (arrow), as well as acute peripancreatic fluid. The gland is hypoperfused but still enhancing, indicating the absence of necrosis. In 1994, the CTSI proposed by Balthazar et al 9 was introduced as an imaging prognosticator that is based on the grade of pancreatic inflammation plus the degree of glandular necrosis. Patients with a CTSI of 7 10 (Figure 3) have an associated 92% morbidity and 17% mortality. Compared with other prognosticators in patients with acute pancreatitis, the accuracy of the CTSI for predicting pancreatitis severity was significantly higher than either APACHE II or C-reactive protein measures; one study with thresholds of CTSI 3, APACHE II 7, and C-reactive protein 150 mg/l found that the sensitivity, specificity, positive and negative predictive values, and overall accuracy were all better by using the CTSI. 10 Although the CTSI Figure 4. MRI of acute pancreatitis. T1-weighted intravenous gadoliniumenhanced axial images through the pancreatic body (A) reveal partial replacement of glandular tissue by low signal collection that expands the retrogastric region. (B) T2-weighted fat-suppressed axial image through the collection reveals the complex nature of the fluid (bright) and solid components depicted by the low signal foci (arrows). (C) Same patient s coronal T1-weighted gadolinium-enhanced image demonstrates the relationship of this postnecrotic pancreatic fluid collection to the duodenal (short arrow) and gastric (arrow) walls, important for endoscopic drainage planning. Figure 6. Acute necrotizing pancreatitis with peripancreatic fat necrosis. Axial CECT image through the pancreatic body region reveals a large amount of peripancreatic fluid extending into the left anterior pararenal space, mesenteric root, and lesser sac. There is enhancement of the pancreatic body (neck and head located on more caudal images). Lower density retroperitoneal fat (arrows) has been incorporated into the collection.

4 1080 MORGAN CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 6, No. 10 Figure 7. Acute necrotizing pancreatitis with pancreatic glandular and peripancreatic fat necrosis. Axial CECT image through the pancreatic tail reveals a geographic area of diminished enhancement (arrow) surrounded by a peripancreatic inflammatory fluid extending in the anterior pararenal space and transverse mesocolon. Low-density retroperitoneal fat (long arrow) has been incorporated into this postnecrotic pancreatic fluid collection. correlates well with local complications, other authors suggest that it is not as effective as the APACHE II score in predicting the length of intensive care unit stay or in the population of patients with necrotizing pancreatitis in predicting survivors versus nonsurvivors. 11 Recognition of the importance of CECT assessment of morphologic changes in the retroperitoneum in patients with acute pancreatitis is shared by radiologists, surgeons, and gastroenterologists alike. CT represents a very reliable method of imaging that is widely available and demonstrates the local extent of inflammation and necrosis in both the pancreas and retroperitoneum Patients with acute pancreatitis may also be assessed by using magnetic resonance imaging (MRI). 15 The MRI findings in patients with acute pancreatitis (Figure 4) were first reported by Lecesne et al 16 in 1999, who described geographic areas of decreased T1 signal on unenhanced MRI that corresponded to areas of pancreatic necrosis depicted with CECT. Other investigators found that the high signal intensity on unenhanced T1-weighted fat-suppressed spoiled gradient echo images corresponded to hemorrhage and correlated with disease severity, 17 3 Figure 8. Inadequate drainage of postnecrotic pancreatic fluid collection. This 63-year-old man was transferred from an outside hospital after placement of a percutaneous 7F catheter, with failure to improve. (A) Axial CECT image through the pancreatic head region reveals a heterogeneous, aircontaining collection in the retroperitoneum. Note 7F drainage catheter (arrow) coursing toward collection from anterior approach. Inflammatory fluid is also seen extending into the right and left anterior pararenal spaces. (B) During endoscopic transgastric drainage of the collection the next day, injection of contrast into the cavity reveals large filling defects (arrows) representing solid necrotic debris that would not pass through the smallbore catheter. (C) Two weeks after placement of transgastric double pigtail catheters and irrigation, noncontrast axial CT through the retroperitoneal cavity reveals near complete evacuation of its contents. The patient underwent noncontrast CT because of renal failure.

5 October 2008 IMAGING OF ACUTE PANCREATITIS AND ITS COMPLICATIONS 1081 Figure 9. Acute peripancreatic fluid collection. A 22-year-old woman had onset of nausea, vomiting, and abdominal pain 24 hours before admission. CECT of the abdomen reveals nonorganized inflammatory fluid extending throughout the left retroperitoneum from the tail of pancreas region. There is no glandular necrosis. and that the sensitivity of MRI for acute pancreatitis might surpass CT as a result of increased detection of minor peripancreatic inflammation on T2-weighted fat-suppressed images. An MR severity index equivalent to the CTSI was established by using dynamic 3-dimensional T1-weighted spoiled gradient echo gadolinium-enhanced images. 18 In addition, the added benefit of main pancreatic and bile duct evaluation with magnetic resonance cholangiopancreatography provides for the complete assessment of patients with suspected acute pancreatitis. Secretin-enhanced magnetic resonance cholangiopancreatography might have a role in assessment of pancreatic duct leak in the setting of acute pancreatitis, and MRI may also be indicated specifically to assess drainability of the complex retroperitoneal collections associated with acute pancreatitis by depicting the relative amounts of liquid versus solid components. The new morphologic classification in patients with acute pancreatitis more than 1 week after onset was proposed by the Working Group in 2007 to better stratify patients at risk for complications. Acute pancreatitis is thus divided into acute interstitial edematous pancreatitis (Figure 5) and acute necrotizing pancreatitis. The necrotic process might be isolated pancreatic gland necrosis, peripancreatic fat necrosis (Figure 6), or both (Figure 7). Acute Necrotizing Pancreatitis The clinical importance of pancreatic necrosis has been stressed for decades. 1 3 Although the minority (approximately 20%) of patients with acute pancreatitis present with the severe form of disease, these are the patients most likely to have a significant degree of pancreatic necrosis. As the amount of pancreatic necrosis increases, there is a greater likelihood of pancreatic duct disruption. 19 The complications of pancreatic necrosis account for 70% 86% of deaths caused by acute pancreatitis. 20 On CECT, pancreatic necrosis is generally depicted as 1 or more focal or geographic areas of nonenhancing pancreatic parenchyma. 21 Pancreatic gland necrosis is typically accompanied by varying degrees of peripancreatic fat necrosis. However, in the hyperacute state, pancreatic necrosis might not be evident up to 48 hours after onset of symptoms, and thus the Working Group suggests that disease severity be stratified by clinical parameters within the first week and by imaging thereafter. Potential imaging pitfalls resulting in overestimation of pancreatic necrosis with CECT include apparent diminished enhancement values in patients with normal fatty infiltration of the pancreas, diffuse parenchymal edema in patients with less severe interstitial pancreatitis, and small intrapancreatic focal fluid collections that may mimic regions of necrosis. 22 In the proposed classification, acute necrotizing pancreatitis may refer to pancreatic gland necrosis as in years past or may to peripancreatic fat necrosis in the absence of glandular necrosis. On CECT, retroperitoneal fat necrosis typically appears as a low attenuation (often near-fluid density) collection, generally with minimal heterogeneity. 23 However, there are no specific CT or MRI features available that can diagnose extrapancreatic fat necrosis, a pathologic entity. Infected pancreatic necrosis remains defined as culture positivity of infected pancreatic and/or peripancreatic necrotic tissue. Infected necrosis occurs in 36% 71% of all patients with pancreatic gland necrosis, typically arises in the second to third week after the onset of severe acute pancreatitis symptoms, and is polymicrobial. 20 On imaging, infected necrosis may be indicated by development of gas within a complex retroperitoneal collection; however, proof of infection is achieved by fine-needle aspirate with culture, because infected collections might not contain gas. As percutaneous and endoscopic drainage tech- Figure 10. Infected postnecrotic pancreatic fluid collection. Patient presented with acute pancreatitis approximately 3 weeks earlier. CECT through the level of the pancreatic tail reveals multifocal moderately marginated collections surrounding the pancreas and enhancement of the pancreatic body (arrow). Each collection contains dependent air bubbles dispersed through the viscous peripancreatic fluid. The predominantly peripancreatic postnecrotic collection is poorly contained, with gas extending to the periphery (short arrows). The gas is indicative of infection in most cases, although spontaneous fistulization to bowel might give rise to air within postpancreatitis retroperitoneal collections.

6 1082 MORGAN CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 6, No. 10 niques evolved during the late 1990s, conversion of previously sterile necrotic collections commonly occurred when evacuation of liquid components through small-bore catheters was achieved, but solid material remained in the retroperitoneum. 24 On CECT, these partially drained, secondarily infected collections frequently demonstrated interspersed air among the solid necrotic debris (Figure 8). Of note, a pitfall in the imaging assessment of partially drained necrotic collections is that air might be introduced during flushing of catheters and thus mimics infection with gas-forming organisms. Fluid Collections Associated With Acute Pancreatitis Acute peripancreatic fluid collection is the new term for acute fluid collection. This represents enzyme-rich pancreatic juice located predominantly adjacent to the gland (Figure 9) that lacks a wall and arises within 48 hours in 30% 50% of patients with acute pancreatitis. The majority of acute peripancreatic fluid collections remain sterile and resolve spontaneously within 2 4 weeks. Postnecrotic pancreatic fluid collection is the new term for an enzyme-rich pancreatic collection that contains both fluid and Figure 11. WOPN. (A) CECT through the mid-body region of the pancreas reveals enhancing glandular tissue in the head and tail region (arrows), with replacement of the mid-body by a low attenuation collection. The poorly marginated acute inflammatory fluid extends into the transverse mesocolon and bilateral anterior pararenal spaces. The patient was treated in the intensive care unit with supportive measures. (B) Same patient 10 days later. CECT through a similar level once again reveals enhancement of remaining pancreas, with replacement of the central gland by low attenuation. There is partial septation within the collection, and enhancement on the periphery suggests that granulation tissue is beginning to wall off the collection. (C) CECT obtained 5 weeks later shows replacement of the central gland by well-demarcated WOPN. A second collection in the transverse mesocolon is seen more anteriorly. This collection, although homogeneous and low in attenuation, does not reflect a simple pseudocyst because it replaces portions of the gland and arose from necrosis. (D) Same patient 3 months after initially presenting with severe acute pancreatitis. The unenhanced CT demonstrates the walled off collection; a portion of the necrotic pancreas (sequestrum) is visible as a slightly more dense structure (arrows) in the posterior portion of the collection.

7 October 2008 IMAGING OF ACUTE PANCREATITIS AND ITS COMPLICATIONS 1083 necrotic contents. This entity is best described as a combination of initial pancreatic glandular and/or retroperitoneal fat necrosis accompanied by acute peripancreatic fluid that, over time, undergoes liquefactive necrosis. When this occurs, the collection becomes more homogeneous and low in attenuation on CECT. These postnecrotic pancreatic fluid collections might become infected (Figure 10). It is critically important that postnecrotic pancreatic fluid collections not be confused with pseudocysts arising from acute pancreatitis, despite a sometimes similar low attenuation appearance on CECT. To differentiate, postnecrotic collections replace portions of the pancreas. The depiction of solid components within these Figure 13. Infected pseudocyst. (A B) Successively caudal axial CECT images through the inferior pancreatic head region reveal a low attenuation fluid collection, with less well-defined irregular walls. This lesion was drained surgically and contained frankly purulent material. Figure 12. Pancreatic pseudocyst. A 45-year-old man with pancreas divisum, 5 weeks after onset of acute pancreatitis. (A) Axial CECT image demonstrates a focal, well-circumscribed low attenuation collection extending anteriorly from the main pancreatic duct (arrow) in the body/tail junction. (B) Same patient s coronal reformatted CT image demonstrates the cyst location in a predominantly extrapancreatic, anterior location. Communication with the main pancreatic duct (demonstrated in A) should be noted because the lesion would be more amenable to successful endoscopic drainage rather than percutaneous approach. collections is better on T2-weighted MRI than on CECT. 25 If allowed to evolve over time without intervention, eventually postnecrotic pancreatic fluid collections become what is now referred to as walled off pancreatic necrosis. Walled off pancreatic necrosis (WOPN) replaces formerly used terms of organized pancreatic necrosis, pseudocyst associated with necrosis, and central cavitary necrosis. These collections require 4 weeks or more to form and contain variable amounts of solid necrotic debris within a well-defined retroperitoneal collection (Figure 11). As was the case with surgical pancreatic necrosectomies in the past, the longer an intervention can be postponed with supportive clinical measures in patients with severe acute pancreatitis, the more liquefactive necrosis can

8 1084 MORGAN CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 6, No. 10 Figure 14. Relationship of nomenclature: Atlanta Classification vs proposed revisions. occur. This delay resulted in better demarcation between viable and necrotic tissue at surgery. In the past, evolving necrotic collections, now termed WOPN, have been mistaken for pseudocysts. This error results in inadequate drainage planning and ultimately might lead to treatment failure. Just as with acute postnecrotic pancreatic fluid collections, it is critical to recognize that in patients with WOPN, CECT and MRI show replacement of pancreatic tissue by the collection. Even when it is necessary to follow WOPN with unenhanced CT (in the case of acute pancreatitis being complicated by renal failure), the pancreas sequestrum and retroperitoneal fat necrosis might be visualized (Figure 11D). Surgical, percutaneous, and endoscopic procedures 26 can be performed on WOPN collections, with successful outcomes when measures to remove the necrotic debris are undertaken. Pancreatic pseudocyst was defined by the Atlanta Symposium in 1992 as a collection of pancreatic juice contained by granulation tissue that required 4 weeks to form and contained little or no necrosis. That definition remains the same. Most pseudocysts resolve spontaneously within weeks, especially when small. On CT, pseudocysts arising from acute pancreatitis are welldefined, homogenous, low attenuation thin-walled collections that lie adjacent to, or occasionally within, an otherwise normal-appearing pancreas (Figure 12). The identification of ductal communication is important for management of pseudocysts, and imaging should be directed toward assessment of this feature. According to the new Working Group definition, pancreatic pseudocysts should be described as noninfected or infected (suppurative). Infected or suppurative pseudocyst is the new name for what had been described in the Atlanta Symposium as a pancreatic abscess. An infected pseudocyst is a circumscribed collection of pus near the pancreas that requires at least 4 weeks to form and contains little or no necrosis. On CECT (Figure 13), the wall of the infected pseudocyst is thicker and more irregular than that of a sterile pseudocyst. This type of collection should be differentiated from infected postnecrotic pancreatic fluid collection and infected WOPNs. These latter collections contain significant amounts of pancreatic glandular or retroperitoneal solid material that liquefies over time at a variable rate. To summarize the differences in nomenclature between the 1992 Atlanta Symposium and that proposed by the Acute Pancreatitis Working Group definitions (Figure 14), the former term acute fluid collection is now acute peripancreatic fluid collection. Acute peripancreatic fluid collections may contribute to postnecrotic pancreatic fluid collections that represent pancreatic gland necrosis, peripancreatic retroperitoneal fat necrosis, or both. Both acute fluid collections and postnecrotic pancreatic/ peripancreatic fluid collections occur immediately and are the preferred term used to describe collections less than 4 weeks after onset of acute pancreatitis. These collections may be sterile or infected. Pancreatic pseudocysts require at least 4 weeks to form, and whether sterile or infected, they arise from acute peripancreatic fluid collections, are generally located adjacent to but outside the pancreatic gland, and do not replace portions of the pancreas. WOPN requires at least 4 weeks to form and represents a mature postnecrotic pancreatic fluid collection with a defined wall. WOPN collections may be sterile or infected. Other complications arising from acute pancreatitis are depicted on CECT and include gastric outlet obstruction, pseudoaneurysm formation, segmental portal hypertension, retroperitoneal hemorrhage, spontaneous fistulization, colon necrosis, and renal obstruction. Indicators of multisystem organ failure such as pulmonary edema and pleural effusions, renal swelling and perirenal edema, or ascites may be seen with CECT or MRI and have been incorporated into a modified version of Balthazar s CTSI. 27 In summary, acute pancreatitis remains a common clinical entity that may be initially diagnosed in small community hospitals or tertiary medical centers. The widespread availability and robust reproducibility of CT have resulted in incorporation of the CECT findings in the definition of this disease according to the 2007 Acute Pancreatitis Working Group. Appropriate use of terms describing the varied collections that arise in patients with acute pancreatitis is critical, and the conveyance of the imaging findings to primary care physicians, gastroenterologists, interventional radiologists, and surgeons is essential for management decision making in these patients. References 1. Balthazar EJ, Freeny PC, vansonnenberg E. Imaging and intervention in acute pancreatitis. Radiology 1994;193: Banks PA. Acute pancreatitis: medical and surgical management. Am J Gastroenterol 1994;89:S78 S Bradley EL. A clinically based classification system for acute pancreatitis: summary of the International Symposium on Acute Pancreatitis, Atlanta, GA, September 11-13, Arch Surg 1993;128: Baron TH, Morgan DE. Current concepts: acute necrotizing pancreatitis. N Engl J Med 1999;340: Besselink M, van Santvoort H, Witteman B, et al. Management of severe acute pancreatitis: it s all about timing. Curr Opin Crit Care 2007;13: Bollen T, van Santvoort H, Besselink M, et al. The Atlanta Classification of acute pancreatitis revisited. Br J Surg 2008;95:6 21.

9 October 2008 IMAGING OF ACUTE PANCREATITIS AND ITS COMPLICATIONS Bollen T, Besselink M, van Santvoort H, et al. Toward an update of the Atlanta classification on acute pancreatitis. Pancreas 2007;35: Besselink M, van Santvoort H, Bollen T, et al. Describing computed tomography findings in acute pancreatitis with the Atlanta Classification: an interobserver agreement study. Pancreas 2006;33: Balthazar EJ, Robinson DL, Megibow AJ, et al. Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990;174: Gürleyik G, Emir S, Kilicoglu G, et al. Computed tomography severity index, APACHE II score, and serum CRP concentration for predicting the severity of acute pancreatitis. JOP 2005;6: Triantopoulou C, Lytras D, Maniatis P, et al. Computed tomography versus acute physiology and chronic health evaluation II score in predicting severity of acute pancreatitis: a prospective, comparative study with statistical evaluation. Pancreas 2007; 35: Vriens PW, van de Linde P, Slotema ET, et al. Computed tomography severity index is an early prognostic tool for acute pancreatitis. J Am Coll Surg 2005;201: Leung TK, Lee CM, Lin SY, et al. Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome. World J Gastroenterol 2005;11: Ju S, Chen F, Liu S, et al. Value of CT and clinical criteria in assessment of patients with acute pancreatitis. Eur J Radiol 2006;57: Miller FH, Keppe AL, Dalal K, et al. MRI of pancreatitis and its complications: part I, acute pancreatitis. Am J Roentgenol 2004; 183: Lecesne R, Taourel P, Bret PM, et al. Acute pancreatitis: interobserver agreement and correlation of CT and MR cholangiopancreatography with outcome. Radiology 1999;211: Pamuklar E, Semelka RC. MR imaging of the pancreas. Magn Reson Imaging Clin N Am 2005;13: Arvanitakis M, Delhaye M, De Maertelaere V, et al. Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis. Gastroenterology 2004;126: Paulson EK, Vitellas KM, Keogan MT, et al. Acute pancreatitis complicated by gland necrosis: spectrum of findings on contrastenhanced CT. Am J Roentgenol 1999;172: Bradley EL, Allen K. A prospective longitudinal study of observation versus surgical intervention in the management of necrotizing pancreatitis. Am J Surg 1994;161: Kivisaari L, Somer K, Standertskjold-Nordenstam CG, et al. A new method for the diagnosis of acute hemorrhagic-necrotizing pancreatitis using contrast enhanced CT. Gastrointest Radiol 1984; 9: Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002;223: Morgan DE, Stanley RJ. The pancreas. In: Lee JKT, Sagel SS, Stanley RJ, et al, eds. Computed body tomography with MRI correlation. Philadelphia, PA: Lippincott, Williams and Wilkins, 2006: Hariri M, Slivka A, Carr-Locke DL, et al. Pseudocyst drainage predisposes to infection when pancreatic necrosis is unrecognized. Am J Gastroenterol 1994;89: Morgan DE, Baron TH, Sith JK, et al. Pancreatic fluid collection prior to intervention: evaluation with MR imaging compared with CT and US. Radiology 1997;203: Baron TH, Thaggard WG, Morgan DE, et al. Endoscopic therapy of organized pancreatic necrosis. Gastroenterology 1996;111: Mortele KJ, Wiesner W, Intriere L, et al. A modified CT severity index for evaluating acute pancreatitis: improved correlation with patient outcome. Am J Roentgenol 2004;183: Address requests for reprints to: Desiree E. Morgan, MD, UAB Department of Radiology, JTN322, 619 S 19th St, Birmingham, AL dmorgan@uabmc.edu; fax: The author discloses no conflicts.