Acute pancreatitis (AP) is a common gastrointestinal tract disease that occurs due to cellular injury and inflammation of the pancreas and is characterized by the abrupt onset of deep epigastric pain and elevated levels of lipase or amylase levels in the blood [1, 2]. Acute pancreatitis is increasing globally; it is one of the most common gastrointestinal causes of hospitalization in the United States and is associated with significant morbidity, mortality, and substantial health care cost [3–5].

The most common causes of acute pancreatitis are gallstones (about 42%) and chronic alcohol use (about 21%), while less frequent causes are hypertriglyceridemia, post-endoscopic retrograde cholangiopancreatography, hypercalcemia, trauma, infection, and idiopathic [6, 7].

The diagnosis of acute pancreatitis requires at least two of the following three criteria: (1) Typical abdominal pain (acute onset severe, persistent, epigastric, and left upper quadrant abdominal pain); (2) Threefold elevation in pancreatic enzymes activity (serum lipase and serum amylase); and (3) Imaging (computerized tomography [CT], magnetic resonance imaging [MRI], ultrasound) findings that are consistent with acute pancreatitis [8].

Based on pathological changes, onset, and severity, acute pancreatitis is classified in Table 38.1 [3, 8–16].

Treatment of acute pancreatitis should be individualized depending on the severity of the disease, causative etiology, presence of complications of severe acute pancreatitis, and coexisting disorders. Management of acute pancreatitis is divided into three broad categories:

A. Initial medical management

B. Endoscopy therapy

C. Surgical therapy

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