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KEY POINTS

KEY POINTS

  • The most common causes of acute pancreatitis are gallstones and alcohol, followed by medications, hypercalcemia, hypertriglyceridemia, postendoscopic retrograde cholangiopancreatography (ERCP), and trauma. 10% to 25% of cases are idiopathic

  • Diagnosis of acute pancreatitis requires two out of three of the following criteria: abdominal pain consistent with acute pancreatitis, elevation of serum lipase and/or amylase to at least three times the upper limit of normal, cross-sectional imaging, and Contrast Enhanced Computed Tomography (CECT) scan or Magnetic Resonance Imaging (MRI) of the abdomen suggestive of acute pancreatitis. Acute pancreatitis is divided into two types: interstitial edematous pancreatitis and necrotizing pancreatitis.

  • Management of acute pancreatitis requires early crystalloid resuscitation and enteral nutrition. Empiric antibiotics are not recommended.

  • ERCP may be considered in gallstone pancreatitis and cholangitis.

  • Peripancreatic and pancreatic fluid collections often resolve without intervention. Drainage procedures should be considered only after the fluid collection has matured radiographically.

INTRODUCTION

Acute pancreatitis (AP) is the most common cause for hospitalization among gastrointestinal diseases, accounting for about 275,000 hospital discharges in the United States in 2009, amounting approximately $2.6 billion per year in inpatient costs, with a median length of stay of 4 days. This reflects a 30% increase from the burden of disease in 2000.1 The overall crude mortality rate of AP was 0.9 per 100,000 in 2016, being 1.1 in males and 0.7 in females.2 The majority of patients (about 80%) have mild disease and are discharged after a few days. Needless to say, it is a disease with an increasing morbidity in patients and burden on the healthcare system, mirroring the rising obesity epidemic and increased rates of gallstone disease.3

PATHOPHYSIOLOGY

AP is a result of activation of local pancreatic enzymes, which leads to a systemic inflammatory cascade, causing tissue damage, organ dysfunction, and eventual failure.4 The phases of AP can be divided into an “early” and a “late” phase. The early phase occurs within one week after onset, and consists of the systemic inflammatory response. Although it is still a debated topic, it is most commonly thought that pancreatitis develops after any mechanism of injury to the pancreatic acinar cells, which allows the pancreatic enzymes to be leaked into the tissue. Lysosomal enzymes (eg, cathepsin B) convert the zymogen trypsinogen to its active form trypsin, which then leads to autoactivation of more trypsin as well as other pancreatic enzymes including phospholipase, chymotrypsin, and elastase.5 These enzymes, once activated in the tissue, result in tissue breakdown leading to AP. Pathological calcium signaling is also key in the pathogenesis of pancreatitis. It contributes to premature trypsinogen activation as well as inhibits effective ATP production. The third cellular event that is central in pancreatitis is impaired autophagy and unfolded protein response (UPR). These mechanisms allow cells to ensure processing of damaged (ie, misfolded) proteins. Deficiency of these mechanisms causes inflammation in ...

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