MICHAEL C. GEOKAS, M.D., Ph.D.; JULIEN L. VAN LANCKER, M.D.; BARBARA M. KADELL, M.D.; HERBERT I. MACHLEDER, M.D.
Acute pancreatitis varies in intensity, from mild edema to generalized fulminant necrosis. Biliary tract disease, alcoholism, and pancreatic trauma are leading causes, other primary conditions accounting for fewer cases. With its high rate of protein synthesis, the pancreas is a "sack of enzymes," and autodigestion is the most plausible pathogenesis for the tissue injury. The activation and release of pancreatic and lysosomal hydrolases is not well understood. The mode of intracellular trypsinogen activation is unknown, although α-chymotrypsin has been detected in blood, ascitic, and pleural effusions. Fat necrosis, glassy edema, hemorrhagic necrosis, and protein-rich fluid exudation are characteristic. Elevated serum or urinary amylase is the most important diagnostic feature. X-ray examination of the abdomen and chest is helpful. Abdominal paracentesis may be useful if perforation of a hollow viscus is suspected. Serum methemalbumin helps in differentiating the edematous from the hemorrhagic form. "Calcium soaps" formation and the release of glucagon and thyrocalcitonin may account for hypocalcemia. Infusion of crystalloids and colloids, analgesics, and nasogastric suction may now be supplemented by peritoneal lavage in hemorrhagic pancreatitis. Exploratory laparotomy is justified in diagnostically doubtful cases.
MICHAEL C. GEOKAS, JULIEN L. VAN LANCKER, BARBARA M. KADELL, HERBERT I. MACHLEDER. Acute Pancreatitis. Ann Intern Med. 1972;76:105–117. doi: 10.7326/0003-4819-76-1-105
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Published: Ann Intern Med. 1972;76(1):105-117.
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