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Acute pancreatitis includes a wide spectrum of disease, from mild self-limiting symptoms to a fulminant process with multiple organ failure and high mortality. Of the approximately 185,000 patients who develop acute pancreatitis each year in the United States, most experience relatively minor episodes of disease characterized by mild parenchymal edema without distant organ dysfunction and an uneventful recovery.1 Severe episodes, however, may involve a progression to extensive pancreatic necrosis, development of the systemic inflammatory response syndrome (SIRS), multiorgan failure, rapid clinical deterioration, and even death.2,3 Although the overall mortality rate with acute pancreatitis is 2–10%, this is primarily related to the 10–30% of patients with severe disease characterized by pancreatic and peripancreatic necrosis.

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Given the wide spectrum of disease seen, the care of patients with pancreatitis must be highly individualized. Patients with mild acute pancreatitis can generally be managed with resuscitation and supportive care. Etiologic factors are sought and treated, if possible, but operative therapy has essentially no role in the care of these patients. In contrast, patients with severe and necrotizing pancreatitis may require maximal nonoperative care and nutritional support in an intensive care unit. On occasion, care of these patients may include wide operative debridement of the infected pancreas or surgical management of local complications of the disease. The precise indications for surgery in patients with pancreatitis have evolved in recent years. Whereas early aggressive debridement was commonly used for all patients with pancreatic necrosis in the past, now most pancreatic surgeons have adopted a more conservative algorithm of selective and delayed pancreatic debridement.4,5 This chapter reviews current management strategies in acute pancreatitis, with particular attention to assessment of disease severity, the timing and routes of supplemental nutrition, the role of prophylactic antibiotics, the indications for and timing of surgery, the methods of pancreatic debridement for necrotizing pancreatitis, and the role of endoscopic and minimally invasive techniques.

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Acute pancreatitis has been attributed to a wide range of etiologic factors, some rare and rather obscure (Table 54-1). Intra-acinar activation of trypsinogen, with subsequent activation of other pancreatic enzymes, is thought to play a central role in the pathogenesis of the disease. Furthermore, ischemia-reperfusion injury is believed to be critical to disease progression. A local inflammatory response in the pancreas is associated with the liberation of oxygen-derived free radicals and cytokines including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor alpha (TNF-α), and platelet-activating factor; these mediators play an important role in the transformation from a local inflammatory response to a systemic illness.

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Table 54-1: Etiologic Factors in Acute Pancreatitis
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