Updated Imaging Nomenclature for Acute Pancreatitis

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Residents Section Structured Review Murphy et al. Imaging Nomenclature for Acute Pancreatitis Residents Section Structured Review Residents inradiology Kevin P. Murphy 1,2 Owen J. O Connor 1,2 Michael M. Maher 1,2 Murphy KP, O Connor OJ, Maher MM Keywords: acute pancreatitis, Atlanta Classification, CT, pancreas imaging, pancreatic collection DOI:10.2214/AJR.13.12222 Received November 5, 2013; accepted after revision April 15, 2014. 1 Department of Radiology, Cork University Hospital, Wilton, Cork, Ireland. Address correspondence to M. M. Maher (m.maher@ucc.ie). 2 Department of Radiology, University College Cork, Cork, Ireland. WEB This is a web exclusive article. AJR 2014; 203:W464 W469 0361 803X/14/2035 W464 American Roentgen Ray Society Updated Imaging Nomenclature for Acute Pancreatitis KEY POINTS 1. CT is used to confirm the diagnosis of acute pancreatitis when the diagnosis is in doubt and to differentiate acute interstitial pancreatitis from necrotizing pancreatitis, which is a key element of the updated Atlanta nomenclature. The acute interstitial variety accounts for 90 95% of cases, with acute necrotizing pancreatitis accounting for the remaining cases. 2. Necrosis due to acute pancreatitis is best assessed on IV contrast-enhanced CT performed 40 seconds after injection. Peripancreatic necrosis is a subtype of necrotizing pancreatitis in which tissue death occurs in peripancreatic tissues. This is seen in isolation in 20% of patients with necrotizing pancreatitis. 3. Simple fluid collections associated with acute interstitial pancreatitis are subdivided chronologically. A collection observed within approximately 4 weeks of acute pancreatitis onset is termed an acute peripancreatic fluid collection (APFC). A collection older than 4 weeks should have a thin wall and is termed a pseudocyst. Both APFCs and pseudocysts can be infected or sterile. 4. Fluid collections associated with necrotizing pancreatitis are labeled on the basis of age and the presence of a capsule. Within 4 weeks of acute pancreatitis onset, a fluid collection associated with necrotizing pancreatitis is termed an acute necrotic collection (ANC) whereas an older collection is termed an area of walled-off necrosis (WON) if it has a perceptible wall on CT. The term pseudocyst is not used in the setting of necrotizing pancreatitis collections. Although an ANC and a (WON can be infected or sterile, infection is far more likely compared with acute interstitial pancreatitis collections. 5. The severity of acute pancreatitis is graded on the basis of the presence of acute complications or organ failure. Mild acute pancreatitis has neither acute complications nor organ failure. Moderate-severity acute pancreatitis is associated with acute complications or organ failure lasting fewer than 48 hours. Severe acute pancreatitis is characterized by single- or multiorgan failure persisting for greater than 48 hours. R adiology plays an integral part in the assessment and management of acute pancreatitis. The 1992 Atlanta Classification System of acute pancreatitis was revised in 2012 by the Atlanta Working Group in conjunction with 11 national and international pancreatic societies [1, 2]. Familiarity with the revised nomenclature is essential for accurate communication of imaging findings. In this article, we summarize the updated nomenclature and illustrate corresponding imaging findings using relevant cases. Disease Epidemiology Acute pancreatitis remains a common reason for hospital admission, with a prevalence of 10 50 per 100,000 people per year [3 7]. Furthermore, the incidence of acute pancreatitis is increasing. Per-patient mortality has improved, but population mortality from acute pancreatitis remains around 6 18 per million per year [3 7], with a per-case mortality rate of approximately 6%. Pathophysiologic Basis Gallstones and alcohol account for the majority of cases of acute pancreatitis [3, 5, 7 9]. Interestingly, a cause is not found in up to one third of cases [8]. The typical clinical history is one of acute constant severe epigastric pain that radiates through to the back. There may be associated vomiting, abdominal distention, tenderness, tachycar- W464 AJR:203, November 2014

Imaging Nomenclature for Acute Pancreatitis Fig. 1 Axial T2-weighted image from MRCP study in 26-year-old woman with gallstone-associated acute interstitial pancreatitis shows gallstones in gallbladder (arrowhead) and common bile duct (arrow). dia, dehydration, or pyrexia. The presence of at least two of the following three conditions is required to fulfill the clinical criteria for acute pancreatitis: acute upper abdominal pain consistent with acute pancreatitis, serum amylase or lipase of at least three times the normal level (ranges: lipase, 30 210 IU/L; amylase, 30 110 IU/L), or typical CT findings [2, 10, 11]. Regardless of the cause, cellular injury of the exocrine acinar cells leads to intracellular digestive enzyme activation (trypsin and proteases predominantly). After enzyme activation, cellular damage leads to systemic release of digestive enzymes, inciting edema, ischemia, and potentially necrosis and liquefaction. This in turn incites a cytokine cascade worsening local inflammation and complications and potentially leading to a systemic inflammatory response syndrome (SIRS) with potential for organ failure. Acute pancreatitis is divided into two phases: early and late [2, 12]. The early phase of acute pancreatitis lasts for 1 week and is characterized by activation of the cytokine cascade with resultant SIRS. SIRS is present when the patient exhibits two or more of the following: heart rate greater than 90 beats/min, temperature less than 36 C or greater than 38 C, respiratory rate greater than 20/min, PCO 2 less than 32 mm of mercury, or WBC less than 4 or greater than 12 10 9 /L. Persisting systemic signs of inflammation or local complications constitute late-phase acute pancreatitis. This begins from the end of week 1 after symptom onset and lasts for several weeks or even months. The late phase is rarely seen in mild acute pancreatitis. Treatment of patients during the Fig. 3 Coronal CT reconstruction image in 59-year-old man with acute interstitial pancreatitis shows peripancreatic fat stranding (arrowheads), and two small acute peripancreatic fluid collections (arrows) are visible. Fig. 4 CT image in 43-year-old man with alcoholassociated necrotizing pancreatitis shows parenchymal (arrow) and peripancreatic (arrowheads) necrosis. Fig. 2 Axial IV contrast-enhanced CT image in 46-year-old man with acute interstitial pancreatitis shows small acute peripancreatic fluid collection (arrows), mild diffuse enlargement of pancreas, and surrounding fat stranding. AJR:203, November 2014 W465

Murphy et al. Fig. 5 CT image in 36-year-old woman with pseudocyst shows contents of pseudocyst are simple in appearance (arrowhead), and thin capsule is observed (arrow) after episode of acute interstitial pancreatitis. early phase of acute pancreatitis is largely based on clinical parameters, but imaging is particularly important to guide treatment of acute pancreatitis during the late phase. Imaging Approach CT is the imaging modality of choice to assess acute pancreatitis and identify associated local complications. Routine CT use is, however, not warranted to confirm the diagnosis or to assess severity. Imaging is not required for the diagnosis of acute pancreatitis if the patient has an appropriate history of abdominal pain and sufficiently elevated serum amylase or lipase. CT can be used to confirm the diagnosis when one Fig. 6 Axial contrast-enhanced CT image in 44-year-old woman with acute necrotic collection shows contents are of mixed attenuation, consistent with complex contents (arrows). of two diagnostic criteria are absent in a patient with suspected pancreatitis. CT is indicated to exclude malignancy in patients greater than 40 years old who develop acute pancreatitis for the first time without an identifiable cause. In addition, imaging to assess disease severity is not required if clinical and biochemical parameters indicate that acute pancreatitis is not severe and if the patient shows sufficient clinical improvement over the first 24 hours. The optimal time for assessing acute complications of acute pancreatitis is approximately 72 hours after symptom onset [11, 12]. Contrast-enhanced CT is the modality of choice for this indication. Unenhanced and pancreatic phases (40 seconds after IV contrast administration) are recommended to accurately assess for necrosis and complications. CT can also provide information pertaining to the type and cause of acute pancreatitis and guidance for management. Performance of further CT should be guided by the patient s clinical and biochemical findings, requirement to check catheter position, or response to treatment. CT is used more commonly than ultrasound to guide interventional procedures to treat pancreatic infective complications of acute pancreatitis largely because of the retroperitoneal location of the pancreas. More superficial infected collections can often be accessed with ultrasound guid- A Fig. 7 35-year-old man with gallstone-associated necrotic pancreatitis. A, CT image shows peripancreatic and pancreatic necrosis (arrowheads) along with large acute necrotic collection (ANC) (arrows). B, Follow-up CT image shows two percutaneous drains (arrowheads) have been placed in interim to drain ANC (arrows), which has reduced in size since initial CT. B W466 AJR:203, November 2014

Imaging Nomenclature for Acute Pancreatitis Fig. 8 Axial contrast-enhanced CT image in 40-year-old woman with necrotizing pancreatitis shows walled-off necrosis with heterogeneous contents (arrow). No gas is seen within collection to suggest infection. ance. Percutaneous drains can be upsized to enable minimally invasive retroperitoneal necrosectomy (step-up approach), where required [7, 13]. Ultrasound and MRI are adjuncts to CT in the appraisal and management of acute pancreatitis. They are predominantly used for the diagnosis of cholelithiasis or cholodocholithiasis and in the assessment of the contents and internal architecture of collections (Fig. 1). Imaging Appearance Differentiating Acute Interstitial Pancreatitis From Necrotizing Pancreatitis Contrast-enhanced CT is used to evaluate the severity and type of acute pancreatitis, particularly in cases in which the Fig. 9 Ultrasound image in 37-year-old man with acute necrotic collection (ANC) shows complex collection as evidenced by internal echogenic debris within ANC (arrows). severity of acute pancreatitis appears moderate or severe or necrosis is suspected. In acute interstitial pancreatitis, the pancreatic parenchyma enhances homogeneously, the peripancreatic fat usually shows some stranding, and a peripancreatic fluid collection may be seen (Figs. 2 and 3). In patients with necrotizing acute pancreatitis, three subtypes can be seen: necrosis of pancreatic parenchyma with sparing of peripancreatic tissues (5%), necrosis of peripancreatic tissue with parenchymal sparing (20%), or involvement of both (75%) [2, 12, 14] (Fig. 4). Patients with peripancreatic necrosis alone have a better prognosis than those with parenchymal involvement but not as good as patients with acute interstitial pancreatitis. CT can be indeterminate for the classification of acute pancreatitis because of heterogeneous pancreatic enhancement, and in this setting repeated CT studies after an interval of between 5 and 7 days should be considered. CT best detects parenchymal necrosis around 72 hours after symptom onset. After unenhanced and pancreatic phase imaging, an area of necrosis is seen as a relatively heterogeneous focus with intermediate attenuation but with no enhancement after contrast administration. After approximately 1 week, the necrotic zone becomes better demarcated and attenuation decreased as its contents liquefy [2, 12]. The percentage of necrotic parenchyma should be estimated because it has Fig. 10 Ultrasound image in 46-year-old woman with walled-off necrosis shows collection is mildly complex with internal echoes (arrows). A definite capsule is evident posteriorly (arrowheads). Fig. 11 Coronal T2-weighted image acquired at MRCP in 54-year-old man with pseudocyst shows internal contents are simple in appearance. Some irregularity of capsule wall (arrows) is seen. AJR:203, November 2014 W467

Murphy et al. Fig. 12 Axial contrast-enhanced CT image in 58-year-old man with necrotizing pancreatitis shows gas-containing infected walled-off necrosis (WON) anterior to left kidney adjacent to pancreatic body and tail (arrow). Further WON is seen posterior to left kidney (arrowhead) that does not contain gas pockets. prognostic significance. Peripancreatic necrosis most commonly involves retroperitoneal fat but is more difficult to detect than parenchymal necrosis. Contrast-enhanced CT features include areas of heterogeneous peripancreatic enhancement that contain liquefied low-attenuation and nonliquefied intermediate-attenuation components. < 4 Weeks APFC Interstitial edematous pancreatitis > 4 Weeks pseudocyst Acute pancreatitis Collections Associated With Acute Interstitial Pancreatitis Collections associated with acute interstitial pancreatitis are subclassified on the basis of the length of time between symptom onset and development of the collection, the presence of a wall surrounding the collection, or the presence of infection. In the initial 4 weeks after development of acute interstitial pancreatitis, a nonencapsulated fluid seen surrounding the pancreas should be termed an acute peripancreatic fluid collection (APFC) [2] (Figs. 2 and 3). On CT, the contents are uniformly hypoattenuating, devoid of solid components, and nonenhancing in appearance. The walls are imperceptible and conform to adjacent structures. APFCs usually resolve spontaneously and do not normally require drainage. After approximately 4 weeks, if the collections persist, a nonepithelialized capsule encompasses these fluid collections and can be observed on CT. Simple collections that have developed perceptible walls within 4 weeks of symptom onset in the setting of APFCs can be characterized as pseudocysts on imaging (Fig. 5). Again, as for APFCs the contents should be simple in appearance. An infected APFC or pseudocyst is uncommon but should be suspected on imaging if gas is seen within the collection. Fluid collections associated with acute interstitial pancreatitis should only be located in peripancreatic tissues. If a collection has an intraparenchymal component then by definition it must be related to necrotizing pancreatitis. Hence, use of the term intraparenchymal pseudocyst is no longer recommended. < 4 Weeks ANC Necrotizing pancreatitis, pancreatic necrosis, or peripancreatic necrosis Fig. 13 Axial contrast-enhanced CT image in 41-year-old woman with infected gas-containing walled-off necrosis shows percutaneous drain in position (arrow). Splenic vein is thrombosed with resultant venous collaterals in left upper quadrant and epigastrium related to stomach (arrowheads). > 4 Weeks WON Collections Associated With Necrotizing Pancreatitis Fluid collections occurring in or around the pancreas within 4 weeks of the onset of necrotizing pancreatitis are termed acute necrotic collections (ANCs) [2] (Figs. 4, 6, and 7). On imaging, ANCs may be observed within or surrounding the pancreas or both. An ANC is characterized on CT by the presence of a heterogeneous collection containing hemorrhage, fat, or necrotic fat occurring in the presence of acute necrotic pancreatitis. ANCs can appear homogeneous and nonenhancing during the first week after symptom onset, but after 1 week, liquefied contents become more obvious. Over time, an enhancing wall develops around an ANC, and if 4 weeks have elapsed since symptom origin, the collection is termed an area of walledoff necrosis (WON) [2] (Fig. 8). The internal contents of an ANC or WON are complex because of the presence of necrotic tissue that results in variable attenuation on CT. MRI or ultrasound may be required to confirm the Fig. 14 Flowchart shows key terminology in new Atlanta pancreatitis nomenclature. Initial differentiation is into interstitial edematous and necrotizing pancreatitis. Details of their associated collections are also outlined. The 4-week time frame for alteration in collection type is approximation and not only criterion used to define evolution. APFC = acute pancreatic fluid collection, ANC = acute necrotic collection, WON = walled-off necrosis. W468 AJR:203, November 2014

Imaging Nomenclature for Acute Pancreatitis nature of the contents and help differentiate an ANC or WON from an APFC or pseudocyst (Figs. 9 11). Communication with the pancreatic duct may also be evident on CT or MRI. This may alter management but does not affect lesion classification. Infection affects the classification of acute pancreatitis. Infection is more likely in an ANC or WON than in an APFC or pseudocyst. Terms such as phlegmon, pancreatic abscess, organized necrosis, sequestration, or necroma should no longer be used. The presence of gas within a collection is highly suggestive of infection (Figs. 12 and 13). If clinical findings are concordant or needle-guided aspiration confirms the presence of infection, these collections are classified as an infected ANC or infected WON depending on the time frame. Air within a collection can be misinterpreted as an abscess if there is communication between the collection and the gastrointestinal tract. Suspicion for infection should therefore be correlated with the patient s clinical examination and biochemical profile and, if necessary, percutaneous fine-needle aspiration should be used to obtain a fluid sample for confirmation [2, 7, 11 13]. Aspiration has a false-negative rate of approximately 10%. If pus is aspirated, percutaneous drain insertion should be performed for the treatment of an infected collection (Figs. 7B and 13). Severity of Acute Pancreatitis Acute pancreatitis severity is divided into mild, moderate, and severe varieties. The parameters used to prescribe these divisions are the presence of organ failure or the presence of local or systemic complications [2, 15]. The new guidelines recommend assessment of renal, cardiovascular, and respiratory system dysfunction via the Modified Marshall Scoring System [2]. CT assessment is of crucial importance in evaluating for local complications and hence stratification of severity. In mild pancreatitis, no end-organ dysfunction or complications are present. Most cases of mild acute pancreatitis are of the acute interstitial variety, have a good prognosis, and usually do not require CT [2]. Moderate severity pancreatitis has organ failure that lasts for fewer than 48 hours and may or may not have local or systemic complications. Severe pancreatitis is characterized by single- or multiorgan failure that persists for greater than 48 hours. The severity of acute pancreatitis can change over a 24-hour period, leading to alteration in the severity score. Conclusion The updated Atlanta Classification attempts to standardize and clarify the nomenclature used to describe acute pancreatitis to improve communication between care providers and to facilitate comparison of new management strategies for acute pancreatitis and outcome in different centers. A clear distinction is made between acute interstitial pancreatitis and necrotizing pancreatitis. (Fig. 14) Collections associated with acute interstitial pancreatitis are termed APFCs in the first 4 weeks after symptom onset and pseudocysts after approximately 4 weeks, once a capsule develops. On the other hand, collections associated with necrotizing pancreatitis are termed ANCs and WON before and after a capsule forms (approximately 4 weeks after symptom onset). In both ANC and WON, the 4-week time frame is an estimation of the length of time required for the peripheries of the collection to become organized and a perceptible wall to become visible on imaging, but the age of the collection is not an absolute requirement. The updated guidelines also confirm stratification of acute pancreatitis into mild, moderate, or severe varieties according to the presence of organ failure and complications. Finally, another important aspect of the updated Atlanta Classification is the identification of early (1 2 weeks) and late (weeks to months) phases of acute pancreatitis. Familiarity and use of this new terminology by radiologists is key to assessing, staging, and managing patients with acute pancreatitis. This system helps health care providers to standardize treatment, communicate imaging appearances using common terminology, and hopefully improve patient outcomes. References 1. Bradley EL. A clinically based classification 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 2. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta Classification and definitions by international consensus. Gut 2013; 62:102 111 3. Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of acute pancreatitis: a systematic review. Pancreas 2006; 33:323 330 4. Vidarsdottir H, Möller PH, Vidarsdottir H, Thorarinsdottir H, Björnsson ES. Acute pancreatitis: a prospective study on incidence, etiology, and outcome. Eur J Gastroenterol Hepatol 2013; 25:1068 1075 5. Roberts SE, Akbari A, Thorne K, Atkinson M, Evans PA. The incidence of acute pancreatitis: impact of social deprivation, alcohol consumption, seasonal and demographic factors. Aliment Pharmacol Ther 2013; 38:539 548 6. Spanier B, Bruno MJ, Dijkgraaf MG. Incidence and mortality of acute and chronic pancreatitis in the Netherlands: a nationwide record-linked cohort study for the years 1995 2005. World J Gastroenterol 2013; 28:3018 3026 7. Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108:1400 1415 8. Chen Y, Zak Y, Hernandez-Boussard T, Park W, Visser BC. The epidemiology of idiopathic acute pancreatitis, analysis of the nationwide inpatient sample from 1998 to 2007. Pancreas 2013; 42:1 5 9. Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology 2013; 144:1252 1261 10. Sarr MG. IAP guidelines in acute pancreatitis. Dig Surg 2003; 20:1 3 11. Working Party of the British Society of Gastroenterology, Association of Surgeons of Great Britain and Ireland, Pancreatic Society of Great Britain and Ireland, and Association of Upper GI Surgeons of Great Britain and Ireland. UK guidelines for the management of acute pancreatitis. Gut 2005; 54(suppl 3):iii1 iii9 12. Thoeni RF. The revised Atlanta Classification of acute pancreatitis: its importance for the radiologist and its effect on treatment. Radiology 2012; 262:751 764 13. Sarr MG. 2012 revision of the Atlanta Classification of acute pancreatitis. Pol Arch Med Wewn 2013; 123:118 124 14. van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010; 362:1491 1502 15. Dellinger EP, Forsmark CE, Layer P, et al. Determinant-based classification of acute pancreatitis severity: an international multidisciplinary consultation. Ann Surg 2012; 256:875 880 AJR:203, November 2014 W469