ABSTRACT
Acute pancreatitis ranges in severity from a minimal edematous in-flammation, which usually resolves spontaneously and completely, to a fulminant process that can progress to an often fatal, necrotizing hemorrhagic pancreatitis. Mild forms of pancreatitis are manifested by abdominal pain, nausea, vomiting, and anorexia and may be confused with many other gastrointestinal disorders. About 10-20% patients with acute pancreatitis develop severe necrotizing pancreatitis, which is character ized by profound hemodynamic, cardiovascular, pulmonary, renal, hematologic, and metabolic aberrations and is associated with high mortality.12 Total parenteral nutri tion (TPN) and metabolic support are essential in patients with severe acute pancre atitis and should be started as soon as possible when the patient has developed more than two of Ransons prognostic criteria. When prescribing nutrient substrates in acute pancreatitis, consideration must be given to their specific effects on pancreatic enzyme secretion, as well as their general effects on nutritional and metabolic ho meostasis. This chapter deals with the pathophysiology o f acute pancreatitis includ ing the effects o f alcohol, biliary disease, oxygen-derived free radicals, and the role o f pancreatic ischemia in inducing acute pancreatitis. Furthermore, associated meta bolic changes, nutritional support with TPN as an essential component o f the care of these patients, and rationales for the use of TPN, as well as the effects o f the nutrient substrates in this disorder are elaborated.
