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  • Acute pancreatitis is a frequent cause of gastrointestinal-related critical illness.

  • Most cases are caused by alcohol and gallstones; other etiologies include hypertriglyceridemia, post-ERCP pancreatitis, hypercalcemia, trauma, infections, and medications.

  • Two of the following three criteria establish the diagnosis of acute pancreatitis: sudden onset of characteristic abdominal pain; serum amylase and/or lipase above three times normal; pancreatic inflammation on imaging studies.

  • There are two types of acute pancreatitis—interstitial edematous and necrotizing. The former has pancreatic enlargement with diffuse pancreatic and peripancreatic inflammation. The latter has necrosis of pancreatic and/or peripancreatic tissue, in addition to inflammatory changes.

  • Early crystalloid administration in fluid-responsive patients is important in the management of acute pancreatitis.

  • Early enteral nutrition has been validated as an important component of the management of acute pancreatitis; avoiding enteral feeding and/or use of parenteral nutrition is not recommended.

  • There is no role for prophylactic antibiotics in the management of acute pancreatitis; however, broad spectrum antibiotics (eg, carbapenems) are indicated in the presence of documented or suspected pancreatitic infection.

  • Endoscopic retrograde cholangiopancreatography (ERCP) is indicated in patients with acute gallstone pancreatitis with cholangitis and those with pancreatic duct disruption.

  • Endoscopic debridement is superior to open necrosectomy for the management of mature, walled-off fluid collections.

Acute pancreatitis is currently the most frequent gastrointestinal cause of hospital admissions in the United States with a total of 275,000 admissions in 20091 and approximately $2.2 billion in annual health care costs.2 The overall mortality among patients with acute pancreatitis is around 5%, but patients who develop severe acute pancreatitis have mortality rates as high as 15%3 and even higher when multiorgan failure is present. Appropriate intensive care management of these patients and a multi-disciplinary approach play a very important role in treatment of those patients who develop severe acute pancreatitis. In 2012, a revised version of the original Atlanta classification was published that focused on defining the severity of acute pancreatitis and classification of pancreatic and peripancreatic fluid collections.4


Acute pancreatitis is believed to be triggered by an increase in the intraductal pressure or direct injury to acinar cells from metabolic or toxic stimuli which leads to breakdown of the junctional barrier between acinar cells and leakage of pancreatic fluid and enzymes into the interstitial space.5 Intrapancreatic activation of proteolytic enzymes leads to autophagy and autodigestion of acinar cells.6 Lysosomal enzymes such as cathepsin B initiate the activation of trypsinogen to trypsin which then leads to activation of more trypsin as well as other pancreatic enzymes including phospholipase, chymotrypsin, and elastase.7 The acinar tissue death leads to an intense systemic inflammatory response syndrome (SIRS) caused by the release of activated pancreatic enzymes and mediated by cytokines, immunocytes, and the complement system. Inflammatory cytokines (such as tumor necrosis factor) cause macrophages to migrate into tissues distant from the pancreas, including lungs and kidneys. Immunocytes attracted by cytokines released from ...

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