Acute Pancreatitis
Introduction -The most common cause of pancreatitis is gallstones. The second most common cause if alcohol. Pancreatitis can be divided into two categories.
- Edematous acute pancreatitis, which is characterized by acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognizable tissue necrosis
- Necrotizing acute pancreatitis, which is characterized by inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis
Clinical Features - Most patients with acute pancreatitis have acute onset of persistent, severe epigastric abdominal pain. In approximately 50 percent of patients, the pain radiates to the back. Approximately 90 percent of patients have associated nausea and vomiting which may persist for several hours.
Diagnosis - The diagnosis of acute pancreatitis requires the presence of two of the following three criteria
- Acute onset of persistent, severe, epigastric pain often radiating to the back
- Elevation in serum lipase or amylase to three times or greater than the upper limit of normal
- Characteristic findings of acute pancreatitis on imaging (focal or diffuse enlargement of the pancreas on contrast-enhanced abdominal CT or MRI is suggestive of acute pancreatitis. Check out the image below...P is for pancreas and it is quite large in that picture)

Management
- Fluid replacement - Up to Date recommends aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (NS or LR) to all patients with acute pancreatitis. Fluid management needs to be reassessed frequently during the hospital stay. Monitor the vital signs, keep HR <120 and MAP between 65-89 and monitor the BUN as both the BUN at the time of admission and the change in 24 hours since admission can predict mortality. Watch the urine output (should be >0.5 to 1 cc/kg/hour) and try to achieve a reduction in hematocrit with a goal of 35 to 44 percent
- Pain control - Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics. Hydromorphone and Fetanyl are recommended. I remember while studying for the boards that Merperidine was recommended over Morphine because it is believed that Morphine will cause contraction of the Sphincter of Oddi which would exacerbate the pancreatitis. However, Merperidine has a very short half life and can be cumbersome to manage the patient's pain adequately.
- Nutrition - In mild pancreatitis, in the absence of nausea or vomiting, oral feeds can be initiated as soon as the pain is decreasing and inflammatory markers are improving (about 24-48 hours). A low fat, soft diet is recommended. In moderately severe to severe pancreatitis, oral feeding is frequently not tolerated. Patients usually require enteral or parenteral feeding. Early enteral nutrition (within 24 to 48 hours) should be initiated when a patient is transferred to the ICU, or has the development of organ failure, or systemic inflammatory response syndrome (SIRS) persisting for 48 hours. Enteral feeding requires the placement of a jejunal feeding tube beyond the ligament of Treitz. The reason it needs to be beyond the ligament of Trietz is to avoid the duodenal release of cholecystokinin, the hormone that will activate the pancreas. A feed that is high protein and low fat is best to avoid little activation of the pancreas.
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