Acute pancreatitis (AP) is a frequent diagnosis encountered in the emergency department (ED), and is a common disease of the gastrointestinal system. The incidence of AP varies between 4.9 and 73.4 cases per 100,000 worldwide, affecting men and women equally.1,2 The clinical manifestations can vary from mild disease, in which there is involvement of the local pancreatic tissue, to progression into necrosis of the pancreas and multiple organ failure. Approximately 25% of patients with AP develop severe disease with associated multiple organ failure, and require admission to the intensive care unit (ICU).3
Physicians often encounter challenges in adequate identification of the subset of patients that will progress into severe acute pancreatitis (SAP).
The majority of the patients diagnosed with pancreatitis in the ED suffer from mild uncomplicated disease. Swaroop et al.4 reported that, in the United States, approximately 210,000 patients are admitted every year for pancreatitis. Of these patients, 20% to 25% will develop SAP.3,4 SAP alone carries a mortality that ranges from 20% to 40% despite ICU admission and aggressive management.4 Alcohol abuse and gallstone disease are the two most common causes that account for approximately 70% to 80% of the cases.5 Most of the patients will exhibit interstitial pancreatitis rather than necrotizing pancreatitis (85% vs. 15%).5 Organ failure occurs more frequently in patients with necrotizing pancreatitis rather than in the interstitial type (50% vs. 5%–10%). Thus, mortality is going to be higher in that subset of patients (17% vs. 3%).5 Infected necrosis will affect 15% to 20% of the necrotizing pancreatitis population.5
The exact mechanisms that trigger the process involved in AP continue to be somewhat poorly understood. As a general rule, the pathways that lead up to the disease are divided into three phases. First, there is activation of trypsin within the pancreatic acinar cells. During the second phase, inflammation within the pancreatic parenchyma ensues. Last, in the third phase, there is extrapancreatic inflammation that may involve remote organ systems, for example, the lungs, heart, and kidneys. The majority of cases of AP are mild, but in 10% to 20% of the patients, the pathways leading to intra- and extrapancreatic inflammation result in systemic inflammatory response syndrome (SIRS). During SIRS, there is massive and uncontrolled release of cytokines and pancreatic enzymes, which may predispose to multiple organ failure and pancreatic necrosis.5,6
The Atlanta classification of pancreatitis was originated in 1992 as an attempt to offer a universal consensus for the classification and definition of pancreatitis. This classification was revised in 2012; some definitions were modified for a better stratification of the patients and better classification of the severity of the disease. Table 26-1 contains the Atlanta Classification.