Emerg Radiol (2012) 19:237–243DOI 10.1007/s10140-011-1001-4

PICTORIAL ESSAY

The revised Atlanta classification for acute pancreatitis:a CT imaging guide for radiologists

Y. Sheu & A. Furlan & O. Almusa & G. Papachristou &

K. T. Bae

Received: 3 October 2011 / Accepted: 8 November 2011 / Published online: 13 December 2011# Am Soc Emergency Radiol 2011

Abstract Accurate diagnosis and description of the various findings in acute pancreatitis is important for treatment. The original Atlanta classification for acute pancreatitis sought to create a uniform system for classifying the severity of acute pancreatitis as well as common language to describe the various events that can occur in acute pancreatitis. The goal was to allow accurate communication between physicians using standardized language so correct treatment options could be used. Since that time, advances in the understanding of acute pancreatitis as well as improvements in both interventions and imaging have led to criticisms of the system and its abandonment by physicians. A 2007 revision of the Atlanta classifications sought to address many of these issues. This article will explain the changes to the Atlanta classification system and provide pictorial examples of the findings in acute pancreatitis as described by the Atlanta classification system.

Keywords Atlanta classification . Acute pancreatitis .

Acute peripancreatic fluid collection . Pseudocyst . Acute postnecrotic fluid collection . Walled-off pancreatic necrosis

Introduction

Clinical management and treatment of acute pancreatitis is often multidisciplinary involving physicians across the

medical, surgical, pathological, and radiological subspe- cialties; therefore, accurate, standardized terminology is required to ensure proper communication and, ultimately, appropriate patient management and treatment. In 1992, a symposium of international experts was convened in Atlanta, Georgia with the task of standardizing the definitions for acute pancreatitis, its severity, organ failure, and local complications. However, this classification system provided poor interobserver agreement among radiologists [1] and nonstandardized terminology is still widely used [2]. To address the weaknesses of the original classification, a new Working Group classification scheme was introduced in 2007 [3].

The purpose of this pictorial essay is to provide radiologists with a CT imaging guide to understand the changes in terminology introduced by the revised Atlanta classification of acute pancreatitis and encourage the adoption of this standardized terminology.

Subtypes of acute pancreatitis

Interstitial edematous pancreatitis

The pathophysiology of acute pancreatitis usually starts as an initial insult to the acinar cells causing inappropriate intracellular activation of trypsinogen and other digestive or

proteolytic enzymes. These enzymes along with freeY. Sheu (*) : A. Furlan : O. Almusa : K. T. BaeDepartment of Radiology, University of Pittsburgh,200 Lothrop Street, 3950 Presby South Towers, Pittsburgh, PA 15213, USAe-mail: sheuy@upmc.edu

G. PapachristouDepartment of Gastroenterology, University of Pittsburgh,200 Lothrop Street, 3950 Presby South Towers,

Pittsburgh, PA 15213, USA

238 Emerg Radiol (2012) 19:237–243radicals injure the acinar cell and cause a release of cytokines and vasoactive mediators leading to edema as well as apoptosis [4]. The inflammatory response in interstitial edematous pancreatitis is sufficient to cause diffuse edema without being severe enough to cause apoptosis and necrosis. In the 1992 Atlanta classification scheme, interstitial edematous pancreatitis (IEP) was formerly termed interstitial pancreatitis [3].

CT findings of IEP include diffuse or localized enlarge- ment of the pancreas with normal homogenous enhance- ment of the gland itself (Fig. 1). The surrounding peripancreatic fat may have stranding or acute peripancre- atic fluid collections, which will be described later. Prognosis is favorable following conservative treatment.

Necrotizing pancreatitis

The presence of pancreatic necrosis indicates that the previously described inflammatory cascade has progressed to cellular apoptosis. As the cellular integrity of the pancreas crumbles, vascular channels supplying the pan- creas are interrupted. As a result, contrast material cannot reach the necrotic portion of the pancreas, thereby the lack of pancreatic enhancement [5].

On CT, the key differentiating factor between necrotizing pancreatitis (NP) and interstitial edematous pancreatitis is the absence of enhancement in all or part of the pancreas that corresponds to regions of necrosis [6]. The role of the radiologist now lies in determining the extent of necrosis and whether or not superimposed infection is present. The new Working Group semiquantifies the extent of necrosis as being <30%, 30–50% and >50% (Fig. 2). It should be noted that in the early stages of acute pancreatitis, there may not have been adequate time for necrosis to develop. Therefore, if there is a strong clinical suspicion, a repeat study should be

Fig. 2 A 47-year-old man with acute necrotizing pancreatitis. Axial contrast-enhanced CT image shows lack of enhancement within the pancreatic head, neck and portion of the pancreatic body (arrow), consistent with pancreatic necrosis. An acute postnecrotic peripancre- atic fluid collection (open arrow) is also appreciated extending into the lesser sac

Fig. 1 A 55-year-old man with acute interstitial edematous pancreatitis. Axial contrast-enhanced CT image shows an

enlarged, edematous pancreas (arrowheads) with reduced but homogeneous enhancement. Associated peripancreatic fat inflammation (arrows) is present

Fig. 3 A 59-year-old man with acute necrotizing pancreatitis. Axial unenhanced CT image shows the presence of gas within the area of pancreatic necrosis and peripancreatic postnecrotic fluid collection suggestive of infected pancreatic necrosis

Emerg Radiol (2012) 19:237–243 239

Fig. 4 A 45-year-old man with acute pancreatitis, 4 days postsymp- tom onset. Axial contrast enhanced CT image shows normal enhancing pancreatic parenchyma with surrounding heterogeneous fatty pancreatic tissue (arrows) suggestive of peripancreatic necrosis. Please note an acute peripancreatic fluid collection (open arrow) extending into the left anterior pararenal space

Fig. 6 A 40-year-old man with acute interstitial edematous pancre- atitis, 2 days postonset of symptoms. Axial contrast-enhanced CT image demonstrates a low attenuation fluid collection (arrow) anterior to the body of the pancreas; based on the time from symptom onset, this is classified as an acute peripancreatic fluid collection. Please note the presence of extensive mesenteric fat stranding

performed in order to reassess the presence and extent of pancreatic necrosis [7]. In a study performed by Hill et al.,28% of patients with mild acute pancreatitis had no abnormalfindings on CT. However, the same study showed that all CTs were abnormal in cases of severe, acute pancreatitis [8]. A recent multicenter study again confirmed that if imaging is performed early in the course of acute pancreatitis, the imaging findings may underestimate the severity of disease [9]. MRI, including the use of diffusion weighted images, may be more sensitive in detecting cases of mild acute pancreatitis [10].

Currently, infection of pancreatic necrosis is the major risk factor for multiorgan failure in the late phase of acute

pancreatitis. Infection of pancreatic necrosis can be seen in20–30% of patients. Mortality rates of infected pancreatic necrosis are significantly higher than necrosis without infection. While infected necrosis is an indication for surgery, there has been a shift to conservative management of sterile pancreatic necrosis unless there is clinical deterioration [11]. The presence of gas within an area of necrosis is highly suspicious for underlying infection (Fig. 3). In equivocal cases, ultrasound or CT-guided fine needle aspiration can be performed to definitely evaluate the presence of infection [12].

In the new Working Group classification, there has been the introduction of a new entity called “peri-

Fig. 5 Changes in terminology for describing types of acute pancreatitis

Fig. 7 A 54-year-old man withacute necrotizing pancreatitis, a b4 days postsymptom onset.a and b Axial contrast-enhanced CT images acquired at two different levels show mixed solid/fluid collections replacing the pancreatic parenchyma consistent with acute postne- crotic fluid collections. In b, please note the presence of higher attenuation solid compo- nents within the collection and tiny locule of air (arrow) suggesting underlying infection

pancreatic necrosis” in addition to the term necrotizing pancreatitis. This entity was first described by Sakorafas in 1992, and it refers to the necrosis of peripancreatic tissue, believed to be due to the release of lipase from the adjacent inflamed pancreas. Although the presence of peripancreatic necrosis itself does not alter treatment options, patients with isolated peripancreatic necrosis usually have a less severe course than those with pancreatic necrosis [13]. A separate study by Harrison et al., confirmed that surgical management is not altered by the presence of pancreatic versus peripancreatic necrosis [14]. On CT, the presence of peripancreatic necrosis is suggested by the presence of “thickening” of the paracolic gutters and/or the base of the small bowel mesentery, along with fat stranding and involvement of the anterior pararenal spaces (Fig. 4). These changes to the terminol- ogy are illustrated on Fig. 5.

Pancreatic and peripancreatic fluid collections

The time interval between the onset of symptoms and the CT study is important for a correct classification of pancreatic and peripancreatic fluid collections. When a fluid collection is diagnosed within 4 weeks from the onset of symptoms, it should be described as either an acute peripancreatic fluid collection or acute postnecrotic collection. After 4 weeks from symptom onset, fluid collections should be referred to as pancreatic pseudocysts or walled-off necrosis.

Acute peripancreatic fluid collection (APFC)

Acute peripancreatic fluid collections (APFC) can arise in patients with either IEP or NP and can be sterile or

infected. In the 1992 classification scheme, they were previously termed “acute fluid collections.” The forma- tion of these collections is felt to be from rupture of a pancreatic side duct triggered by pancreatic inflamma- tion. Morphologically, they are located predominately adjacent to the pancreas, have no definable wall, and

Fig. 8 A 52-year-old man, 36 days postonset of acute interstitial edematous pancreatitis. Axial contrast enhanced CT image shows a low attenuation fluid collection (arrow) with a thickened well-defined wall arising near the tail of the pancreas, consistent with a pseudocyst. There are no internal solid components and the adjacent pancreatic tissue has been displaced but not replaced

Fig. 9 A 67-year-old man with acute necrotizing pancreatitis. Axial contrast-enhanced CT images acquired at the time of presentation (a) and 40 days (b) after onset of symptoms. Image a shows diffuse pancreatic ne- crosis (arrowheads) with an ad- jacent acute postnecrotic fluid collection (arrow). The CT im- age in b shows the development of a thickened wall surrounding the necrotic collection, in keep- ing with walled-off pancreatic necrosis

are confined by the normal peripancreatic fascial planes [15] (Fig. 6). In the case of acute, sterile, peripancreatic fluid collections, treatment is conservative as most of these collections will usually resolve over 2 to 4 weeks. Infected collections require drainage and a diagnostic puncture can be performed if the clinical or imaging findings for infection are equivocal [12].

Acute postnecrotic collection (APNC)

Unlike APFCs, acute postnecrotic pancreatic/peripancreatic fluid collections (APNC) result from the liquefaction of necrotic tissue. As such, they contain variable amounts of fluid and solid components (Fig. 7). They were not specifically defined in the original 1992 Atlanta classifica-

tions; this has led to confusion as there was no standardized way to describe these findings in the original classification system. APNCs may or may not have a connection with the pancreatic ductal system secondary to necrosis and disrup- tion of the main pancreatic duct. As they arise from areas of necrosis, they tend to replace the pancreatic parenchyma, and this is an important clue to distinguish them from pseudocysts and infected pseudocysts [5]. Differentiation of these collections from acute peripancreatic fluid collections is important as the treatment is different. While the former two are usually sterile and can be managed conservatively, postnecrotic fluid collections need to be drained to prevent infection and possible sepsis. New developments in image- guided percutaneous drainage techniques have made such interventions considerably easier [11].

Fig. 10 Changes in terminology describing peripancreaticfluid collections between theoriginal 1992 Atlanta classification and the new2007 Working Group classification

Pancreatic pseudocyst

Fig. 11 A 53-year-old man with a history of chronic pancreatitis. Axial-enhanced CT image shows thrombus within the splenic vein (white arrowheads)

The definition of pancreatic pseudocyst is unchanged from the original Atlanta conference. It represents the evolution of an APFC and occurs 4 weeks after the symptom onset with the formation of a thickened wall. Morphologically, they are described as a round or oval homogenous fluid collection surrounded by a well-defined wall with no associated tissue necrosis within the fluid collection (Fig. 8). It is important to reemphasize that pancreatic necrosis does not evolve into a pseudocyst [1]! The presence of solid components within a fluid collection may be difficult to differentiate, especially, if the collection is at the end stages of liquifactive necrosis. For indetermi- nate cases, MRI may help differentiate between the two [16]. With pancreatic pseudocysts, the current literature indicates that 50% of them will resolve without any intervention especially if small (<6 cm) and asymptomatic [17]. Like APFCs these can be either infected or sterile. The wall of an infected pseudocyst is often thicker and more irregular; infected pseudocysts require drainage. Of note, the term pancreatic abscess, which was originally described

Fig. 12 A 64-year-old man with a history of acute pancreatitis. Axial CT, MIP, and 3D reconstructions show subsequent development of a pseudoaneurysm of the gastroepiploic artery (white arrows)

as a “localized collection of purulent material without significant necrotic material,” has been abandoned because it was both an extremely uncommon finding and because there was misuse of this term in the literature [2].

Walled-off pancreatic necrosis

The term walled-off pancreatic necrosis, WOPN, has been introduced to describe the evolution of a postnecrotic pancreatic fluid collection. Previously, it was referred in the literature as organized necrosis, necroma, or pancreatic sequestration [2]. Just as an APFC evolves into a pseudocyst after 4 weeks, a postnecrotic pancreatic fluid collection turns into walled-off pancreatic necrosis after4 weeks. Over a period of 4 weeks, a thick wall develops without an epithelial lining. In this respect, it resembles a pseudocyst; however, it can be differentiated on CT images by the presence of internal solid components (Fig. 9). Postnecrotic pancreatic fluid collections and WOPN can be treated conservatively if they are sterile. However, infected or symptomatic collections are usually treated with mini- mally invasive surgery or percutaneous drainage [11]. The changes in terminology for pancreatic and peripancreatic fluid collections are summarized on Fig. 10.

Extrapancreatic imaging findings

The biliary tree should be assessed for possible etiologies that may have caused pancreatitis including cholelithiasis, acute cholecystitis, cholodocholithiasis, or biliary obstruction (sphincter dysfunction, stricture, or even lesions). Vascular complications that may arise following pancreatitis include thrombosis of the mesenteric, splenic or portal veins or pseudoaneurysm development (Figs. 11 and 12, respectively) [18]. Often times, systemic inflammatory responses can be seen (e.g., pleural effusion, ascites, hyperenhancement of the adrenal glands, inflammatorylike involvement of peripancre- atic organs—stomach, duodenum, small bowel, colon, spleen, and kidney, and liver) [19].

Conclusions

In summary, the Working Group has recently revised the previous Atlanta classification system and terminology of acute pancreatitis to amend for limitations and inconsisten- cies. Accurate description of CT imaging findings of acute pancreatitis using universally accepted terminology is

crucial to improve communication with clinicians and determine appropriate clinical management of acute pan- creatitis.

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