MICHAEL C. GEOKAS, M.D.. Ph.D.; HAROLD A. BALTAXE, M.D.; PETER A. BANKS, M.D.; JOSEPH SILVA Jr., M.D.; CHARLES F. FREY, M.D.
The exocrine pancreas secretes into the gut on demand more than 20 proteins that are indispensable for digestion. In-vivo autodigestion is prevented by an array of natural safeguards. In acute pancreatitis, inappropriate intrapancreatic activation and release of pancreatic hydrolases occur, but the pathogenetic mechanism of autodigestion is unclear. The release of proteases, lipase and colipase, phospholipase A, vasoactive peptides, and other agents probably accounts for the edema, tissue destruction, fat necrosis, metabolic abnormalities, and complications. Ethyl alcohol abuse, gallstones, trauma, and other common and rare conditions can induce pancreatitis. The patient's outcome can be predicted by certain prognostic signs. Ultrasonography and computerized tomography are invaluable diagnostic tools and magnetic resonance imaging appears promising. Hemodynamic monitoring, intensive care with colloid and crystalloid infusions, correction of electrolyte abnormalities, judicious use of antibiotics, peritoneal lavage, drainage of pancreatic exudation fluids, and surgical intervention require a team approach, especially in patients with multiple complications. Additional research is needed into the pathogenetic mechanism of autodigestion and the design of specific therapies.
MICHAEL C. GEOKAS, HAROLD A. BALTAXE, PETER A. BANKS, JOSEPH SILVA, CHARLES F. FREY. Acute Pancreatitis. Ann Intern Med. 1985;103:86–100. doi: 10.7326/0003-4819-103-1-86
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Published: Ann Intern Med. 1985;103(1):86-100.
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