The RACAP classification system is based on 2 types of pancreatitis (interstitial edematous pancreatitis and necrotizing pancreatitis), 2 overlapping phases, 3 categories, and 4 types of local complications.4,7 The 2 overlapping phases in a patient's dynamic condition with 2 peaks of mortality are the early and late phases. The early phase generally concludes by the end of the first week, although a small minority of patients may experience an extension into the second week. The late phase is characterized by persistence of systemic signs or by the presence of local complications. This is a dynamic phase with respect to individual progression of disease, rather than an arbitrary time point (such as, for instance, 1 week after onset of symptoms). The 3 categories of severity are classified as mild, moderate, and severe. Mild AP is the most common type and is not accompanied by organ failure or local or systemic complications. Mild AP generally resolves within the first week. Moderate AP is defined by the presence of transient organ failure, as well as local complications or exacerbation of comorbidities. Severe AP is defined by persistent organ failure for a period longer than 48 hours.8 The 4 local complications are APFC, pancreatic pseudocysts, ANC, and WON.
Determinant-based classification of acute pancreatitis severity is based on actual local and systemic determinants of severity, rather than descriptions of events correlated with severity.5,9 The local determinant relates to the presence of sterile or infected (peri-) pancreatic necrosis, whereas the systemic determinant relates to transient or persistent organ failure. The presence of both infected (peri-) pancreatic necrosis and persistent organ failure has a greater effect on severity than either determinant alone. The derivation of a classification based on the above principles results in 4 categories of severity: mild, moderate, severe, and critical.
From the data presented in Table 1, it is clear is that there is either a common basis or a fine distinction between the 2 classification systems. Firstly, the description of mild AP is the same in both systems. Confusingly, there, however, are duplicated terms for describing AP in RACAP-defined interstitial edematous pancreatitis with morphologic features and mild AP with severity. The complication APFC is included in the classification of interstitial edematous pancreatitis. Interestingly, there is little mention of the role APFC plays in mild acute pancreatitis.10 It is not clear as to whether or not all local complications are included in RACAP-defined moderate AP. Another common opinion is that both working groups proposed a “moderate” category for classifying severity, characterized by the presence of local complications in sterile (peri-) pancreatic necrosis in DBCAPS and/or transient organ failure.11 Physicians know that local complications are not in fact equivalent with regard to disease severity. The onset of infected pancreatic necrosis often indicates severe disease and is quite different in significance to the onset of an acute peripancreatic collection without infection.12 As demonstrated in the current study, moderate AP accounted for a large proportion of patients, generally as a result of local complications such as APFC. In addition, the primary prognosis was recovery as opposed to disease progression.
The major differences observed when comparing RACAP and DBCAPS are derived from the role of infection in severe AP. The definition of severe AP in RACAP is characterized only by the presence of persistent organ failure.13 Determinant-based classification of acute pancreatitis severity, however, introduced a new category of severe AP known as critical AP, which is classified according to the presence of both infected (peri-) pancreatic necrosis and/or persistent organ failure.14 The severe AP classification focused on patients with a higher risk of mortality because of: persistent organ failure; infected (peri-) pancreatic necrosis, as the onset of infected pancreatic necrosis is most often indicative of severe disease; and prohibitive mortality where both infected pancreatic necrosis and persistent organ failure are present, defined as critical AP.15,16 Our study showed that there is a higher risk of progress for critical AP in DBCAPS when compared with RACAP. Indeed, RACAP should be of limited predictive value in severe cases of infected (peri-) pancreatic necrosis.
Both RACAP and DBCAPS emphasize clinical determinants in their severity estimations, while pathophysiological significance of risk is downplayed, especially with regard to systemic inflammatory response syndrome (SIRS).17 Cytokine cascades are activated by pancreatic inflammation that clinically manifests as SIRS. The sheer complexity of concurrent proinflammatory and anti-inflammatory responses belies a clear understanding of the pathophysiology of the biochemical mechanisms responsible for initiating local and systemic manifestations of the underlying inflammatory process.18 Although SIRS is considered a significant risk for persistent organ failure in severe AP, its role in the classification of AP severity is ambiguous. It is well known that AP is an inflammatory process; thus, a more sophisticated understanding of the dynamic condition should take into account the balance of pro- and anti-inflammatory responses leading to local and systemic complications. Unfortunately, our study did not include pathologic diagnoses and future studies should focus on this aspect.
As presented in Table 2, there is no essential difference in terms of the definitions for (peri-) pancreatic tissue infection, with the exception of the level of detail described. Different definitions of local complications, however, have been proposed by RACAP and DBCAPS. The most important contribution of RACAP is the redefinition of local complications of AP, which is derived from their content, wall, site, and evolution. Through the use of high-resolution computed tomography (CT) scans and an improved understanding of the natural history of local complications, a series of morphologic descriptions have been defined that ensure more consistent and accurate radiologic reports of CT scan results.10 Resolution CT is further able to identify APFC, pancreatic pseudocysts, ANC, and WON.19 It is understood that while RACAP has proposed that infections may develop in the ANC and WON, infection can occur in all 4 lesion types. On the contrary, the most significant contribution of DBCAPS is the distinction between the definitions of sterile peripancreatic necrosis, sterile pancreatic necrosis, infected peripancreatic necrosis, and infected pancreatic necrosis.
The only accurate measure for confirming infected (peri-) pancreatic necrosis, however, is a positive culture and current management of local complications in acute pancreatitis does not recommend early intervention.20 As a result, application of DBCAPS relies heavily on the diagnosis of (peri-) pancreatic necrosis, defined as necrosis in either the pancreatic parenchyma or the peripancreatic fat, or both. Necrosis is identified using contrast-enhanced imaging to visualize areas of nonenhancement.3 Using CT scans alone, differentiation between peripancreatic fat necrosis (less common) and acute peripancreatic fluid collections (quite common) is unreliable, and could lead to overreading.3
This study had several limitations. These include: the restrospective study type, possible bias as a result of admission rate in our hospital, minimal pathophysiological evidence, and additional aspects, such as follow-up data, that were somewhat insufficient. Although none of the tools currently available meet all criteria, every step forward in the classification of acute pancreatitis will improve the development of diagnostic techniques and therapies. It is not surprising that different approaches have yielded such varying results. Clinicians and researchers may need to decide which classification of severity will better meet their needs. Indeed, the comparison and possible combination of multiple tools is one of the best ways to find a new path forward in science. If RACAP and DBCAPS could be combined, a new classification for AP may emerge.
Both the RACAP and DBCAPS classification systems include organ failure and complications as determinants of severity. Revised Atlanta classification refines local complications whereas DBCAPS has modified severity and added a critical AP classification. In accordance with the demands of precision medicine, a combination of the 2 could prove to be significant for both clinical practice and scientific research. Furthermore, a clear demonstration of the pathophysiology of the biochemical mechanisms responsible for initiating local and systemic manifestations will be key to elucidating the morbidity and mortality of AP in the future.
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