R e s i d e n t s ’ S e c t i o n • S t r u c t u r e d R ev i ew O’Connor et al. Complications of Acute Pancreatitis

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

Residents’ Section Structured Review

Residents

inRadiology Owen J. O’Connor 1,2 Julliette M. Buckley 3 Michael M. Maher 1,2 O’Connor OJ, Buckley JM, Maher MM

Keywords: abdominal CT, abdominal MRI, abdominal ultrasound, acute pancreatitis, complications of acute pancreatitis, pancreatic necrosis DOI:10.2214/AJR.10.4339 Received January 26, 2010; accepted after revision July 12, 2010. 1 Department of Radiology, Cork University Hospital, University College Cork, College Rd, Cork, Cork County 0000, Ireland. Address correspondence to O. J. O’Connor ([email protected]). 2 Department of Radiology, Mercy University Hospital, Cork, Ireland. 3 Department of Surgery, Mercy University Hospital, Cork, Ireland.

WEB This is a Web exclusive article. AJR 2011; 197:W375–W381 0361–803X/11/1973–W375 © American Roentgen Ray Society

Imaging of the Complications of Acute Pancreatitis Educational Objectives 1. The Atlanta classification system is most commonly used to classify the severity of acute pancreatitis but does not provide exact radiologic criteria for classifying the complications of acute pancreatitis. A revision of the Atlanta criteria is under way and alternative more specific descriptive terms have been suggested. 2. The severity of acute pancreatitis may be classified radiologically using the CT severity index. This system scores the extent of pancreatic fluid collections and necrosis and has been shown to have prognostic accuracy for the subsequent development of complications. 3. A fluid collection in the setting of acute pancreatitis may be an acute fluid collection, a pseudocyst, or an abscess. 4. Pancreatic necrosis is considered one of the most significant complications of acute pancreatitis because the presence and extent of necrosis help predict the likelihood of future morbidity and mortality. 5. Management of the complications of severe acute pancreatitis is frequently very challenging, requiring a multidisciplinary approach involving the intensivist, medical physician, surgeon, and radiologist. For example, differentiating necrosis from an abscess can be difficult and the expertise of multiple clinicians may be necessary for definitive diagnosis. The distinction between pancreatic necrosis and abscess is important because an abscess has a better prognosis and can be treated with percutaneous drainage, whereas interventional radiology has a limited role or no role in the management of necrosis, with surgery and necrosectomy being necessary in severe cases. Acute pancreatitis may be classified clinically or radiologically. Increasing grades of pancreatic injury are associated with higher

complication rates [1–3]. Complications may be local or remote, acute or delayed, abdominal or systemic. As with the diagnosis of acute pancreatitis, CT is the dominant imaging modality for initially identifying complications and for assessing response to therapy. Epidemiology Acute pancreatitis is associated with a wide variety of complications [4–6] (Table 1). Negative prognostic factors that are associated with an increased likelihood of the development of complications in patients with acute pancreatitis include increasing age, gallstone disease, organ failure on admission, and pancreatic necrosis [5] (Fig. 1). Pancreatic necrosis is considered to be one of the most important complications that can occur, and it is also considered to be the most important indicator of disease severity [7]. Necrosis occurs in 6–20% of patients with acute pancreatitis, with 90% of affected patients developing at least single-organ failure and one third developing an infection [5]. Patients with pancreatitis without necrosis have a 6% morbidity rate and no mortality, but there is an 82% incidence of morbidity and a 23% incidence of mortality in patients with acute pancreatitis complicated by necrosis [1]. Pathophysiology The activation of intraacinar zymogen granules, impeded protein secretion, autodigestion, and cell death with the release of trypsin and proinflammatory mediators leads to the development of acute pancreatitis and its complications [5]. Terminology The Atlanta classification system is most commonly used to clinically classify acute pancreatitis as either mild or severe and it defines many of the complications that may occur [8]. Mild disease is associated with

AJR:197, September 2011 W375

O’Connor et al. TABLE 1: Complications of Acute Pancreatitis

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

Location

Complications

Local

Acute fluid collections, acute pseudocyst, abscess, pancreatic necrosis, disconnected duct, chronic pancreatitis

Remote abdominal

Peritonitis; diabetes; jaundice; cholecystitis; cholangitis; renal, splenic, or portal vein thrombosis; pseudoaneurysm; gastrointestinal bleeding; ileus; splenic complications (pseudocyst, abscess, hemorrhage, infarction, rupture); vascular complications (splenic, gastroduodenal artery); splenic vein thrombosis; and “left-sided portal hypertension,” as described by Mallick and Winslet [20]

Systemic

Systemic inflammatory response syndrome, disseminated intravascular coagulopathy, respiratory failure (adult respiratory distress syndrome, pleural effusion, atelectasis), renal failure, cardiovascular shock, cerebrovascular accident, hypocalcemia, hyperglycemia, hyperlipidemia

Fig. 1—CT of 42-year-old man with acute pancreatitis complicated by necrosis. Contrast-enhanced CT scan shows lack of enhancement of majority of pancreas (arrow). Extensive stranding of peripancreatic fat and ascites are seen. This patient is at risk of disconnection of main pancreatic duct.

minimal organ dysfunction and an uncomplicated recovery [4]. Patients with severe acute pancreatitis have organ failure or systemic complications [4]. The classification of the severity of acute pancreatitis is discussed in greater detail in a review of the imaging of acute pancreatitis [9]. The Atlanta system attempted to standardize the terminology of acute pancreatitis. For example, use of the imaging term “phlegmon” is discouraged because it does not correlate with the presence of either infection or necrosis [3]. Similarly, it is recommended that the term “hemorrhagic pancreatitis” be limited to intraoperative or postmortem settings because most peripancreatic fluid collections contain blood and the presence of hemorrhage does not correlate with the se-

verity or extent of necrosis [3, 10]. Improved imaging has introduced new terms, such as “organized pancreatic necrosis” and “necroma,” which has prompted calls for an updated classification system with better defined radiologic terms [8]. The Atlanta criteria have been subject to criticism regarding the amylase and lipase threshold levels quoted for the diagnosis of acute pancreatitis; the definitions of fluid collections, necrosis, and pseudocysts; and the failure to differentiate temporary from persistent organ failure [8, 11]. The definitions of acute pancreatitis and its complications described by the Atlanta criteria have been shown to be a source of confusion and a revised version is being prepared [8, 12]. Grading of Disease Severity on CT The CT severity index (CTSI) can be used to radiologically grade the severity of acute pancreatitis with good prognostic accuracy [1] (Table 2). This is made possible by the ability of contrast-enhanced CT to directly identify pancreatic necrosis. Patients with mild acute pancreatitis have interstitial inflammation and an intact capillary bed, which should enhance uniformly on contrast-enhanced CT. Pancreatic ische­ mia and necrosis, which are characteristic of severe acute pancreatitis, impair pancreatic enhancement at CT. CT has a sensitivity of 50% and 100% for the presence of minor and extensive pancreatic necrosis, respectively [13]. The CTSI categorizes acute pancreatitis into five grades of increasing severity from A

to E using a 10-point scale. Points are awarded on the basis of the presence of pancreatic enlargement, fat stranding, and collections and the amount of pancreatic necrosis. Patients with a score of zero show no mortality but those with scores of between 7 and 10 have a 17% mortality rate and a 92% incidence of complications. The CTSI is a better indicator of prognosis than Ranson’s score, based on the Ranson acute pancreatitis criteria, and is better able to differentiate interstitial from necrotizing acute pancreatitis than the Acute Physiology and Chronic Health Evaluation II (APACHE II) score [14, 15]. Clinical scoring systems such as the multiple-organ system failure score, Ranson criteria, Glasgow prognostic criteria (Imrie criteria), and APACHE II are also used to grade the severity of acute pancreatitis and to gauge the likelihood of complications developing [2, 3]. However, the clinical usefulness of these scoring systems is not universally accepted and their ability to predict the presence of necrosis or the likelihood of the future development of necrosis remains in doubt [7]. Imaging Findings Imaging of the complications of acute pancreatitis is primarily performed with CT. According to the Atlanta criteria, a fluid collection in the setting of acute pancreatitis may be an acute fluid collection, a pseudocyst, or an abscess [8]. Acute fluid collections occur in the vicinity of the pancreas early in the course of severe acute pancreatitis and do not

TABLE 2: CT Severity Index (CTSI) to Classify the Severity of Acute Pancreatitis Description of Pancreas

CT Grade

No. of Points Assigned for CT Grade

Percentage of Pancreas With Necrosis

No. of Points Assigned for Percentage Necrosis

CTSIa

Normal

A

0

0

0

0

Focal or diffuse enlargement

B

1

0

0

1

Peripancreatic fat abnormalities

C

2

< 30

2

4

Single ill-defined fluid collection

D

3

30–50

4

7

Two or more ill-defined fluid collections

E

4

> 50

6

10

aNote—The CTSI is calculated as the sum of the points for CT grade and the points for percentage necrosis.

W376

AJR:197, September 2011

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

Complications of Acute Pancreatitis Fig. 2—CT of 72-year-old man with acute pancreatitis and acute fluid collections. A, Unenhanced CT scan shows acute fluid collection (arrow) without perceptible wall that is conforming to its surrounding structures anterior to tail of pancreas and left anterior pararenal space. B, Pancreas (arrow) enhanced uniformly after contrast administration, thus showing no evidence of necrosis.

A

B Fig. 3—CT of 56-year-old man with pseudocyst formation after episode of acute pancreatitis. A, Unenhanced CT scan shows large pancreatic pseudocyst (arrow) that is compressing and displacing stomach anteriorly (arrowhead). B, CT image shows pseudocyst as it is being drained under CT guidance with 12-French hydrophilic catheter using trocar technique.

A

B

have a perceptible wall (Fig. 2). These collections often conform to the anatomic spaces in which they reside, may cross the anterior pararenal space, and usually surround the pancreas [16]. Acute fluid collections spontaneously resolve in approximately 50% of patients with acute pancreatitis but progress to form a pseudocyst or an abscess in the remaining 50% of patients [8]. A sterile organized peripancreatic fluid collection containing pancreatic secretions encapsulated by a fibrous wall occurring more than 4 weeks after the onset of symptoms is termed a “pseudocyst” [4]. Although approximately 40% of pancreatic pseudocysts resolve spontaneously, persistent enlargement, infection, hemorrhage, and biliary and gastric obstruction are potential complications that may necessitate intervention [16] (Fig. 3). Pancreatic abscess formation occurs in the vicinity of the pancreas, typically 4–6 weeks after symptom onset; a pancreatic abscess contains pus but little or no necrotic debris [4]. Abscess is seen on CT as a focal area of low attenuation in the vicinity of the pancreas surrounded by a thick wall that may enhance [16]. The presence of bubbles of gas within a collection is considered to be diagnostic of abscess formation by some authors and to be highly suggestive of abscess formation by others [4].

As we await the revised Atlanta criteria, alternative descriptive morphologic terms with good-to-excellent interobserver agreement based on a review of 55 CT examinations in patients with severe acute pancreatitis were suggested [17]. This system describes the extent of pancreatic nonenhancement similar to the CTSI (none, < 30%, 30–50%, > 50%) and the morphology of a collection if present. The morphologic terms describe the location of a collection, encapsulation, contents, displacement of adjacent structures, and presence and shape of gas or presence of an air-fluid level. It is hoped that this system will help clinicians of multidisciplinary teams achieve more consistent agreement regarding diagnosis and management of severe acute pancreatitis and its complications and will limit errors. Pancreatic necrosis is diagnosed on CT if all or part of the pancreas fails to enhance after IV contrast administration [1] (Fig. 4). Pancreatic necrosis may be accompanied by peripancreatic fat necrosis, which is suggested by the presence of pancreatic necrosis associated with a collection containing heterogeneous contents in the vicinity of the pancreas [17]. Necrosis is initially treated medically without surgical or radiologic intervention [17]. Pancreatic necrosis usually develops within 24–48 hours after symptom onset; thus, ear-

ly CT within 12 hours of symptom onset may be falsely reassuring [18]. Contrast-enhanced CT performed 3 days after symptom onset is believed to more accurately detect necrosis than CT examinations performed earlier after symptom onset [7]. Infection is a major complication of pancreatic necrosis—occurring in 30–70% of cases—and is responsible for approximately 80% of deaths in patients with severe acute pancreatitis [16]. Twenty percent of pancreatic abscesses contain gas, therefore, the diagnosis of abscess should be considered when a pancreatic collection contains gas; however, aspiration under image guidance is often necessary for confirmation before definitive intervention [6]. The distinction between pancreatic necrosis and abscess is sometimes difficult, but this distinction is important because an abscess has a better prognosis and can be treated with percutaneous drainage whereas surgery with necrosectomy is more often required for the treatment of necrosis [10]. Another complication observed in the setting of pancreatic necrosis is that of a disconnected main pancreatic duct [19]. Disconnection occurs when a segment of the pancreatic ductal epithelium undergoes necrosis and viable pancreatic tissue becomes isolated from the duodenum. This leads to continuous leakage of pancreatic secretions with consequent

AJR:197, September 2011 W377

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

O’Connor et al.

A

B

C

D

Fig. 4—CT and ultrasound of 44-year-old woman with pancreatitis complicated by necrosis and pseudocyst formation. A, Initial CT scan shows necrosis of pancreatic neck and tail (arrows) and multiple calcified gallstones in gallbladder (arrowhead). B, CT scan obtained 5 weeks after onset of symptoms shows large collection (arrow) in region of pancreatic neck and body. C, Ultrasound image shows that collection (arrow) appears hypoechoic. This finding is consistent with pseudocyst; drain was inserted using transgastric approach. D, Follow-up CT scan confirms that position of drain is satisfactory and pseudocyst is smaller.

Fig. 5—CT and MRCP of 44-year-old man with suspected disconnection of main pancreatic duct. A, CT image shows a zone of pancreatic necrosis (arrow) that measures greater than 2 cm, which isolates viable pancreatic tissue in pancreatic tail from viable tissue in pancreatic head are seen. B, MRCP image shows proximal and distal aspects of pancreatic duct (arrows), but duct cannot be seen in region affected by pancreatic necrosis and pseudocyst formation (arrowhead), thus raising suspicion for presence of disconnection of pancreatic duct.

A

B

inflammation and an increased incidence of infection [19]. Disconnection of the main pancreatic duct is diagnosed by showing an area of pancreatic necrosis of at least 2 cm, viable pancreatic tissue proximal to the necrotic region, and extravasation of contrast material at pancreatography [19] (Fig. 5). Severe acute pancreatitis may be complicated by vascular abnormalities that are a result of enzymatic digestion from pancreatic secretions or infection. Pseudoaneurysm formation is reported to occur in 3.5–10% of patients with acute pancreatitis. The most commonly affected arteries are the splenic (40%) and gastroduodenal (30%) arteries [20] (Fig. 6). Vascular thrombosis is another frequently observed complication of severe acute pancreatitis (Fig. 7). Splenic vein thrombosis is reported to occur in 10–40% of patients with acute pancreatitis and can

lead to imaging features of “left-sided portal hypertension” [20]. Thrombosis of the portal vein may also be associated with hepatic infarction (Fig. 8). Therefore, while reviewing CT scans of a patient with acute pancreatitis, performing a thorough evaluation for vascular complications is vital. Unfortunately, the incidence of recurrence after a single episode of acute pancreatitis is quite high. For example, approximately half of patients who develop acute pancreatitis because of alcohol consumption will experience another episode [21]. This recurrence can precipitate chronic pancreatitis, which not only develops after recurrent episodes of acute pancreatitis but also can occur after a single sentinel event [22]. The main features of chronic pancreatitis on CT are of pancreatic duct dilatation, parenchymal atrophy, and the presence of calcifications [23] (Fig. 9).

W378

Another consequence of repeated episodes of acute pancreatitis is increased radiation exposure. Among patients with suspected abdominal sepsis, those with acute pancreatitis or abscess require the largest number of CT scanner visits, leading to high radiation doses [24] (Fig. 10). However, CT is critical for guiding the management of acute pancreatitis, and as a result the increased use of CT is usually justified in these patients who are typically very ill. The American College of Radiology Appropriateness Criteria [25] suggest that CT is the most appropriate modality for imaging patients with severe abdominal pain, an elevated serum lipase level, and signs of sepsis or shock or failure to improve after 48 hours of treatment. Complementary imaging using ultrasound and MRI should be performed if feasible in the follow-up of collections or before hospital discharge.

AJR:197, September 2011

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

Complications of Acute Pancreatitis

A

B

C

D

E

F

Fig. 6—MRI, ultrasound, CT, and conventional angiography of 54-year-old man with pancreatic pseudocyst who subsequently developed splenic artery pseudoaneurysm and life-threatening hemorrhage. A, Coronal T2-weighted MR image shows large high-signal collection (arrow) consistent with pancreatic pseudocyst. B, On ultrasound image, pseudocyst (arrow) has complex heterogeneous echotexture. C, Unenhanced CT scan of abdomen shows endoscopically placed cyst-gastrostomy drainage catheter in situ for treatment of pancreatic pseudocyst (arrow). D, Follow-up arterial phase CT scan of abdomen shows pseudoaneurysm of splenic artery (arrow) adjacent to drainage catheter. E, Conventional angiography image confirms presence of splenic artery pseudoaneurysm (arrowhead). Pseudoaneurysm was successfully treated by splenic artery embolization with platinum coils. F, Follow-up CT scan shows infarction of spleen (arrowhead) with extensive spray artifact due to coils.

Fig. 7—CT of 40-year-old man with partial superior mesenteric vein thrombosis complicating acute pancreatitis. CT scan shows filling defect in superior mesenteric vein (arrowhead).

Patients with severe acute pancreatitis are at risk of high cumulative effective radiation doses from imaging with CT, therefore, the development of low-dose CT techniques in this population needs to be encouraged. Minimization of radiation exposure in patients with acute pancreatitis can be achieved by limiting

A

B

Fig. 8—CT of 25-year-old woman with acute pancreatitis complicated by thrombosis of right main branch of portal vein and infarction of portions of liver and left kidney. A, There is thrombosis of right main portal vein (arrowhead) and wedge-shaped area of decreased attenuation (arrow) in peripheral aspect of right lobe of liver consistent with infarction. B, Acute fluid collection (arrowhead) is present and infarcts (arrows) are seen in liver and left kidney.

the number of imaging phases—for example, imaging in a single phase during follow-up. New low-dose CT protocols should take advantage of evolving technology that is being developed specifically to limit radiation dose such as iterative reconstruction techniques, which have been reported to reduce abdomi-

nal radiation exposure by 25% compared with filtered back projection [26]. In addition, automatic tube current modulation can reduce radiation exposure from abdominal CT by 78% [27]. Unfortunately, the impact of these techniques has not been investigated specifically in the setting of acute pancreatitis [27].

AJR:197, September 2011 W379

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

O’Connor et al.

Fig. 9—CT of 61-year-old woman with atrophic calcified pancreas as a result of chronic pancreatitis. CT scan shows that pancreas is atrophic and contains numerous calcific densities and that pancreatic duct (arrow) is dilated.

A

B

Fig. 10—CT of 56-year-old man with pancreatic abscess after acute pancreatitis. A, On initial presentation, large heterogeneous fluid collection (arrow) is seen in lesser sac that displaces stomach (arrowhead) anteriorly. B, Abscess (arrowhead) is initially drained percutaneously with 8-French drainage catheter, which was gradually up-sized.

Fig. 11—CT and MRCP of 49-year-old woman with gallstone pancreatitis and acute pancreatic collections. A, CT scan of abdomen depicts large calculus in Hartmann pouch (arrow) and collection in head of pancreas (arrowhead). B, Follow-up coronal MRCP image shows calculus in distal common bile duct (arrow) and fluid collections in both flanks (arrowheads) that developed during interval between CT and MRCP. C, Axial MRCP image confirms choledocholithiasis (arrow). D, CT scan shows bilateral drainage catheters within collections (arrowheads), which contain air.

Ultrasound is potentially a valuable tool in the management and follow-up of various complications of acute pancreatitis, facilitating rapid bedside imaging, diagnostic aspiration, and drain insertion [16] (Fig. 4). Endoscopic ultrasound can be useful for characterizing pancreatic collections before intervention and for selecting the collections most likely to benefit from catheter drainage; endoscopic ultrasound can also help to eliminate the risk of wrongly classifying cystic pancreatic neoplasms as “pseudocysts” and the resultant inappropriate drainage of these lesions [26]. Fat-saturated T2-weighted MRI is also useful for characterizing collections before drainage by confirming the absence of significant volumes of solid debris. MRI is superior to CT and ultrasound in this regard, with the advantage of not requiring IV contrast administration [28, 29] (Fig. 11). Conclusion Acute pancreatitis is associated with a wide variety of complications affecting the pancreatic gland, pancreatic duct, and surrounding vasculature. The role of the radiologist in the imaging of acute pancreatitis and its complications is to select the most appropriate imag-

W380

A

B

C

D

ing techniques and to diagnose local complications that will guide management decisions and reduce morbidity.

system for acute pancreatitis: summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch Surg 1993; 128:586–590 5. Nagar AB, Gorelick FS. Epidemiology and pathophysiology of acute pancreatitis. In: Forsmark CE, ed. Pancreatitis and its complications. Totowa, NJ: Humana, 2005:3–15 6. Merkle EM, Görich J. Imaging of acute pancreatitis. Eur Radiol 2002; 12:1979–1992 7. Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002; 223:603–613 8. Bollen TC, van Santvoort HC, Besselink MG, et al. The Atlanta classification of acute pancreatitis revisited. Br J Surg 2008; 95:6–21

References 1. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990; 174:331–336 2. Tran DD, Cuesta MA. Evaluation of severity in patients with acute pancreatitis. Am J Gastroenterol 1992; 87:604–608 3. Millar FH, Keppke AL, Balthazar EJ. Pancreatitis. In: Gore GM, Levine MS, eds. Textbook of gastrointestinal radiology, 3rd ed. Philadelphia, PA: Elsevier, 2008:1885–1915 4. Bradley EL III. A clinically based classification

AJR:197, September 2011

Downloaded from www.ajronline.org by 37.44.207.114 on 01/17/17 from IP address 37.44.207.114. Copyright ARRS. For personal use only; all rights reserved

Complications of Acute Pancreatitis 9. O’Connor OJ, McWilliams S, Maher MM. Imaging of acute pancreatitis. AJR 2011; 197:W221– W225 10. Haaga JR. The pancreas. In: Haaga JR, Lanzieri CF, Gilkeson RC, eds. CT and MR imaging of the whole body, 4th ed. St. Louis, MO: Mosby, 2003:1395–1486 11. Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006; 101:2379–2400 12. Talukdar R, Vege SS. Recent developments in acute pancreatitis. Clin Gastroenterol Hepatol 2009; 7(suppl 11):S3–S9 13. Berger HG, Maier W, Blaock S, Buchler M. How do imaging methods influence the surgical strategy in acute pancreatitis? In: Malfertheiner P, Ditschuneit H, eds. Diagnostic procedures in pancreatic disease. Berlin, Germany: SpringerVerlag, 1986:54–60 14. Basterra G, Alvarez M, Marcaide A, Delgado E, Díaz de Otazu R, García Campos F. Acute pancreatitis: evaluation of the prognostic criteria of the latest Balthazar tomographic classification. Rev Esp Enferm Dig 1999; 91:433–438 15. Lankisch PG, Warnecke B, Bruns D, et al. The APACHE II score is unreliable to diagnose necrotizing pancreatitis on admission to hospital. Pan-

creas 2002; 24:217–222 16. Maher MM, Lucey BC, Gervais DA, Mueller PR. Acute pancreatitis: the role of imaging and interventional radiology. Cardiovasc Intervent Radiol 2004; 27:208–225 17. van Santvoort HC, Bollen TL, Besselink MG, et al. Describing peripancreatic collections in severe acute pancreatitis using morphologic terms: an international interobserver agreement study. Pancreatology 2008; 8:593–599 18. Freeny PC. Incremental dynamic bolus computed tomography of acute pancreatitis. Int J Pancreatol 1993; 13:147–158 19. Sandrasegaran K, Tann M, Jennings SG, et al. Disconnection of the pancreatic duct: an important but overlooked complication of severe acute pancreatitis. RadioGraphics 2007; 27:1389–1400 20. Mallick IH, Winslet MC. Vascular complications of pancreatitis. JOP 2004; 5:328–337 21. Pelli H, Sand J, Laippala P, Nordback I. Longterm follow-up after the first episode of acute alcoholic pancreatitis: time course and risk factors for recurrence. Scand J Gastroenterol 2000; 35: 552–555 22. Pelli H, Lappalainen-Lehto R, Piironen A, Järvinen S, Sand J, Nordback I. Pancreatic damage after the first episode of acute alcoholic pancreatitis and its association with the later recurrence rate.

Pancreatology 2009; 9:245–251 23. Luetmer PH, Stephens DH, Ward EM. Chronic pancreatitis: reassessment with current CT. Radiology 1989; 171:353–357 24. Meeson S, Alvey CM, Golding SJ. Justifying multidetector CT in abdominal sepsis: time for review? Br J Radiol 2009; 82:190–197 25. American College of Radiology Website. ACR Appropriateness Criteria: October 2008 version. www.acr.org/SecondaryMainMenuCategories/ quality_safety/app_criteria.aspx. Published October 2008. Accessed May 10, 2010 26. Prakash P, Kalra MK, Kambadakone AK, et al. Reducing abdominal CT radiation dose with adaptive statistical iterative reconstruction technique. Invest Radiol 2010; 45:202–210 27. Udayasankar UK, Li J, Baumgarten DA, Small WC, Kalra MK. Acute abdominal pain: value of non-contrast enhanced ultra-low-dose multi-detector row CT as a substitute for abdominal radiographs. Emerg Radiol 2009; 16:61–70 28. Kalra MK, Maher MM, Sahani DV, Digmurthy S, Saini S. Current status of imaging of pancreatic diseases. J Comput Assist Tomogr 2002; 26:661–675 29. Morgan DE, Baron TH, Smith JK, Robbin ML, Kenney PJ. Pancreatic fluid collections prior to intervention: evaluation with MR imaging compared with CT and US. Radiology 1997; 203:773–778

F O R YO U R I N F O R M AT I O N

AJR Web Exclusives are peer-reviewed journal articles selected by the Editor in Chief for immediate full-text Web-only publication based on their timeliness and critical importance to current medical imaging issues. Abstracts for these articles will be published in the print and online monthly issues of AJR.

AJR:197, September 2011 W381