Diagnosis of severe acute pancreatitis can be difficult; indeed, 30 to 40 per cent of fatal cases pass undetected until postmortem discovery. Outcome is highly unpredictable at the onset, as severe local, regional, and/or remote complications may arise subsequently. The pathogenesis is still poorly understood so that truly specific treatment is lacking; management strategies and their timing remain a matter of controversy.

Most cases (80-90 per cent) of acute pancreatitis are mild, self-limiting, and morphologically characterized by edematous interstitial inflammation that resolves rapidly following a period of bowel rest, pain control, and fluid/electrolyte replacement. The disease course is seldom complicated and overall mortality is below 3 per cent. However, 10 to 20 per cent progress to a devastating illness, which is classified as severe acute pancreatitis on the basis of a fatal attack or failure to settle on simple supportive therapy because of local and/or systemic complications. Morphological hallmarks are extensive pancreatic and retroperitoneal inflammation with superimposed patchy or generalized areas of necrosis and hemorrhage in the pancreas and surrounding tissues. The propensity and degree of severity of both local and remote complications are closely linked to the magnitude of the inflammatory reaction and the presence and extent of ensuing regional necrosis ( Begerefa/

1988). Severe acute pancreatitis still carries a mortality between 10 and 20 per cent.

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