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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 27  |  Issue : 2  |  Page : 164-168

Revised atlanta classification for acute pancreatitis – A pictorial depiction


1 Department of Radio Diagnosis, Kamineni Institute of Medical Sciences, Narketpally, Telangana, India
2 Department of General Surgery, DM Wayanad Institute of Medical Sciences, Wayanad, Kerala, India
3 Department of General Surgery, Government Medical College, Thrissur, Kerala, India

Date of Submission10-Jun-2021
Date of Decision04-Sep-2021
Date of Acceptance06-Sep-2021
Date of Web Publication15-Nov-2021

Correspondence Address:
Dr. Ajith Vettuparambil
Department of General Surgery, DM Wayanad Institute of Medical Sciences, Wayanad - 673 577, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ksj.ksj_32_21

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  Abstract 


Introduction: There are various classifications for clinical presentation of acute pancreatitis. However, most of them are not standardised. Aims and Objectives: The revised Atlanta classification is designed to precisely describe patients with acute pancreatitis, standardise terminology across specialties and help in treatment planning. Materials and Methods: The revised Atlanta classification was analysed to describe the features of acute pancreatitis. Results: Acute pancreatitis is now divided into two distinct subtypes: necrotising pancreatitis and interstitial oedematous pancreatitis (IEP). Use of the terms such as acute pseudocyst and pancreatic abscess is currently being discouraged. Four distinct collection subtypes are identified based on the presence of pancreatic necrosis and the time elapsed since the onset of pancreatitis which include acute peripancreatic fluid collections, pseudocysts, acute necrotic collections (ANCs) and walled-off necrosis (WON). Conclusions: The updates in classification and terminology of local complications have clarified confusing terms from the original Atlanta classification. In this article, we report an image-rich guide to the revised Atlanta classification system to improve stratification of the patients both for clinical care and research.

Keywords: Acute pancreatitis, interstitial oedematous pancreatitis, necrotising pancreatitis, the revised Atlanta classification


How to cite this article:
Athikayula AR, Vettuparambil A, Chirukandath R. Revised atlanta classification for acute pancreatitis – A pictorial depiction. Kerala Surg J 2021;27:164-8

How to cite this URL:
Athikayula AR, Vettuparambil A, Chirukandath R. Revised atlanta classification for acute pancreatitis – A pictorial depiction. Kerala Surg J [serial online] 2021 [cited 2021 Nov 30];27:164-8. Available from: http://www.keralasurgj.com/text.asp?2021/27/2/164/330396




  Introduction Top


The 1992 original Atlanta classification for AP created consensus-based terminology for types, severity and complications of AP.[1] Although the Atlanta classification has been useful, some of the definitions have been proven to be ambiguous. A better understanding of the pathophysiology of organ failure and necrotising pancreatitis and their outcomes, as well as improved diagnostic imaging, has made it necessary to revise the Atlanta classification.[2] The revised Atlanta classification (RAC) was established in 2012 to clarify terminology and more specifically categorise AP and its complications. This consensus classification defines criteria for the diagnosis of acute pancreatitis, differentiates the types of acute pancreatitis (interstitial oedematous pancreatitis [IEP] and necrotising pancreatitis), classifies the severity of acute pancreatitis into three categories and defines the morphology seen on imaging of pancreatic and peripancreatic collections that arise as complications.[2],[3] This article has been prepared based on our experiences in classifying the patients presenting with acute pancreatitis according to the revised Atlanta system.


  Computed Tomography Presentation of Different Stages of Acute Pancreatitis Top


We have used the revised definitions of morphological features of acute pancreatitis.[2]

Interstitial oedematous pancreatitis

It is acute inflammation of the pancreatic parenchyma and peripancreatic tissues but without recognisable tissue necrosis. The contrast-enhanced computed tomography (CECT) criteria are pancreatic parenchyma enhancement by intravenous contrast agent and no findings of pancreatic and peripancreatic necrosis. We present a 45-year-old male with acute interstitial oedematous pancreatitis (IEP). CECT shows a mild enlargement of the body and tail of the pancreas with homogeneous enhancement [Figure 1].
Figure 1: Contrast-enhanced computed tomography of the patient with interstitial oedematous pancreatitis. Shows mild enlargement of body and tail of the pancreas (white arrow) with homogeneous enhancement. There is peripancreatic fluid collection and inflammation in the form of fat stranding (black arrow)

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Necrotising pancreatitis

It is an inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis. CECT criteria are lack of pancreatic parenchymal enhancement by intravenous contrast agent and/or presence of findings of peripancreatic necrosis (see below – ANC and walled-off necrosis [WON]). We present three cases. First is a 50-year-old male with acute necrotising pancreatitis with acute necrotic collection (ANC). CECT shows diffuse non-enhancement of the pancreas. Pancreatic parenchyma is replaced by non-enhancing necrotic components [Figure 2].
Figure 2: Contrast-enhanced computed tomography of the patient with acute necrotising pancreatitis shows pancreatic parenchyma replaced by non-enhancing necrotic components (white arrow) and peripancreatic heterogeneous collection (black arrow). Small fluid collection and inflammation noted in the left perinephric space and right anterior pararenal space

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Second is a 42-year-old male with acute necrotising pancreatitis in pancreatic and peripancreatic areas. CECT findings are shown in [Figure 3].
Figure 3: Contrast-enhanced computed tomography of the patient with acute necrotising pancreatitis. Note heterogeneous areas of non-enhancement in tail of the pancreas (black arrow) and non-enhancing and non-encapsulated collection in the retroperitoneum and lesser sac (white arrow)

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Third is a 55-year-old male patient with pancreatic and peripancreatic necrosis. The CT scan shows ANC with acute necrotising pancreatitis [Figure 4].
Figure 4: Contrast-enhanced computed tomography showing pancreatic and peripancreatic necrosis. Note non-enhancement of pancreas and replacement of pancreatic tissue with heterogeneous collection (black arrow) with areas of fat within. The collection is seen extending in the peripancreatic regions as well (white arrow)

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Acute peripancreatic fluid collection

It is peripancreatic fluid associated with interstitial oedematous pancreatitis with no associated peripancreatic necrosis. This term applies only to areas of peripancreatic fluid seen within the first 4 weeks after onset of interstitial oedematous pancreatitis and without the features of a pseudocyst. The CECT criteria include occurrence in the setting of interstitial oedematous pancreatitis, homogeneous collection with fluid density confined by normal peripancreatic fascial planes and no definable wall encapsulating the collection adjacent to the pancreas (no intrapancreatic extension). We present a case of acute peripancreatic fluid collection in a 39-year-old male. The body of pancreas appears oedematous. There is non-encapsulated homogeneous fluid collection in the peripancreatic region [Figure 5].
Figure 5: Contrast-enhanced computed tomography picture of acute peripancreatic fluid collection. The body of pancreas appears oedematous (black arrow) and non-encapsulated homogeneous fluid collection in the peri-pancreatic region is noted, predominantly extending anterior to the pancreas (white arrow). Inflammatory changes are noted surrounding the fluid collection

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Pancreatic pseudocyst

It is an encapsulated collection of fluid with a well-defined inflammatory wall outside the pancreas with minimal or no necrosis. This entity usually occurs 4 weeks after the onset of interstitial oedematous pancreatitis. CECT criteria include well-circumscribed, usually round or oval, homogeneous fluid density, no non-liquid component, well-defined wall, that is, completely encapsulated. Maturation usually requires >4 weeks from the onset of acute interstitial oedematous pancreatitis.

We present a 30-year-old male with pseudocyst of more than 4 weeks duration following acute pancreatitis. CT showed acute oedematous interstitial pancreatitis with pseudocyst [Figure 6].
Figure 6: Computed tomography scan showing a well-defined homogeneous encapsulated collection with smooth margins anterior and inferior to head of the pancreas with no gas pockets within indicating a sterile pseudocyst (black arrow)

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Acute necrotic collection

It is a collection containing variable necrosis that can involve the pancreatic parenchyma and/or the peripancreatic tissues. CECT criteria include occurring only in the setting of acute necrotising pancreatitis, heterogeneous and non-liquid density of varying degrees in different locations (some appear homogeneous early in their course) and no definable wall encapsulating the collection. Location is intrapancreatic and/or extrapancreatic.

We present two cases, first a 37-year-old male with acute necrotising pancreatitis of more than 4 weeks duration and sterile ANC. The head of pancreas shows non-enhancement and appears heterogeneous. Non-encapsulated peripancreatic heterogeneous collection with areas of fat noted with surrounding inflammatory changes suggestive of ANC [Figure 7].
Figure 7: (a) (Axial view) and (b) (coronal view): Contrast-enhanced computed tomography of acute necrotic collection. The head of pancreas is non-enhancing and appears heterogeneous (black arrows). Non-encapsulated peripancreatic heterogeneous collection (white arrow in Figure 7a)

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The second is a 29-year-old male with infected acute necrotising pancreatitis of less than 4 weeks with infected acute necrotic intrapancreatic collection. The CT scan findings are shown in [Figure 8]a and [Figure 8]b.
Figure 8: (a and b) Contrast-enhanced computed tomography picture of acute necrotising pancreatitis showing bulky pancreas with intrapancreatic heterogeneous collection with multiple pockets of gas within (black arrow). There is non-encapsulated peripancreatic heterogeneous collection with surrounding inflammatory changes noted in peripancreatic and right sub-hepatic space suggestive of acute necrotic collection (white arrow)

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Walled-off necrosis

It is a mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has developed a well-defined inflammatory wall. WON usually occurs >4 weeks after onset of necrotising pancreatitis.

We present two cases: one is a 23-year-old male with acute necrotising pancreatitis of more than 4 weeks with sterile WON. Pancreas appears bulky and with heterogeneous enhancement [Figure 9].
Figure 9: Contrast-enhanced computed tomography of acute necrotising pancreatitis with sterile walled-off necrosis. Pancreas appears bulky with heterogeneous enhancement. Encapsulated heterogeneous necrotic collection is noted in body and tail of the pancreas (black arrows)

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Second is a 37-year-old male with infected WON in acute necrotising pancreatitis. Second is a 37 year old male with infected WON in acute necrotising pancreatitis who had well encapsulated heterogeneous collection involving pancreatic and peripancreatic regions with pockets of gas [Figure 10].
Figure 10: Contrast-enhanced computed tomography of acute necrotising pancreatitis and infected walled-off necrosis. Well-encapsulated heterogeneous collection involving pancreatic and peripancreatic regions with pockets of gas within surrounding inflammatory changes suggestive of walled-off necrosis with infection (black arrow)

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  Discussion Top


The RAC provides a comprehensive classification of AP that enabled standardised reporting of research and communication between clinicians worldwide. It offers new data regarding aetiology, pathophysiology, severity and radiologic description of pancreatic and peripancreatic collections.[3]

Acute pancreatitis can be subdivided into two types: IEP and necrotising pancreatitis. The clinical symptoms of IEP usually resolve within the fifth week.[2],[3] About 5–10% of patients develop necrosis of the pancreatic parenchyma, the peripancreatic tissue or both. The impairment of pancreatic perfusion and signs of peripancreatic necrosis evolve over several days, which explains why an early CECT may underestimate the eventual extent of pancreatic and peripancreatic necrosis.[4] The development of secondary infection in pancreatic necrosis is associated with increased morbidity and mortality.[2],[3],[4],[5],[6]

Local complications are acute peripancreatic fleri collection, pancreatic pseudocyst, ANC and WON.[2],[4] The morphologic features of acute pancreatitis are well delineated by high resolution, multi-detector CECT and form the basis of the new, more objective definitions for the local complications of acute pancreatitis.[3],[5] Exacerbation of pre-existing co-morbidity, such as coronary artery disease or chronic lung disease, precipitated by acute pancreatitis is defined as a systemic complication.[2] Organ failure is defined as a score of ≥2 using the Modified Marshall scoring system.[7]

The classification (RAC) defines three degrees of severity: mild acute pancreatitis, moderately severe acute pancreatitis and severe acute pancreatitis.[8] Patients with mild acute pancreatitis usually do not require pancreatic imaging, and mortality is very rare. Moderately severe acute pancreatitis may resolve without intervention (as in transient organ failure or acute fluid collection) or it may require prolonged specialist care (as in extensive sterile necrosis without organ failure).[9] The mortality of moderately severe acute pancreatitis is far less than that of severe acute pancreatitis.[2],[9]


  Conclusion Top


The updates in classification and terminology of local complications have clarified confusing terms from the original Atlanta classification. In this article, we report an image-rich guide to the RAC system to improve stratification of the patients both for clinical care and research.

Acknowledgements

We acknowledge both Department of Radiodiagnosis and Department of General Surgery, Mysore Medical College and Research Institute, Mysore. We also acknowledge the help of Dr. Gilsa E S, Dr. Sharlet Shabu Pappachan and Akhil T Anil for completing this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Bradley EL 3rd. 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;128:586-90.  Back to cited text no. 1
    
2.
Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al. Classification of acute pancreatitis-2012: Revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-11.  Back to cited text no. 2
    
3.
Colvin SD, Smith EN, Morgan DE, Porter KK. Acute pancreatitis: An update on the revised Atlanta classification. Abdom Radiol 2019;45:1222-31.  Back to cited text no. 3
    
4.
Foster BR, Jensen KK, Bakis G, Shaaban AM, Coakley FV. Revised Atlanta classification for acute pancreatitis: A pictorial essay. Radiographics 2016;36:675-87.  Back to cited text no. 4
    
5.
Morgan DE. Imaging of acute pancreatitis and its complications. Clin Gastroenterol Hepatol 2008;6:1077-85.  Back to cited text no. 5
    
6.
Banks PA, Gerzof SG, Langevin RE, Silverman SG, Sica GT, Hughes MD. CT-guided aspiration of suspected pancreatic infection: Bacteriology and clinical outcome. Int J Pancreatol 1995;18:265-70.  Back to cited text no. 6
    
7.
Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung CL, Sibbald WJ. Multiple organ dysfunction score: A reliable descriptor of a complex clinical outcome. Crit Care Med 1995;23:1638-52.  Back to cited text no. 7
    
8.
Petrov MS, Windsor JA. Classification of the severity of acute pancreatitis: How many categories make sense? Am J Gastroenterol 2010;105:74-6.  Back to cited text no. 8
    
9.
Renner IG, Savage WT 3rd, Pantoja JL, Renner VJ. Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. Dig Dis Sci 1985;30:1005-18.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]



 

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